Eye Training

Eye Training

(The brain? Ehh, we're not so sure.)

Clinical skill requires keen observation to even raise a question.

Spotting glitches in walking can require an awareness of easy to miss relationships. Eye training. We have, in our other books,

beaten into the ground that we do NOT swing the leg in walking. We swing the thigh. We, then, decelerate the swinging thigh which gets passed by the trailing foreleg & foot, a dampened double pendulum.

The psoas starts the thigh into swing with enough energy to go on well after that oomph is put in. Stopping the two linked pendulums before they reach a natural pendulum end point does two important things. 1. It protects us from chaotic patterns. 2. The swing energy & momentum is transferred to the pelvis just as the stance leg needs a boost over its vertical pendulum (metronome-like) to rise past the top. But we may be presented with subtle

issues that are compensated into near invisibility. We don't walk with defects if possible; we avoid them. Our tricky dodges often get disease names. :-( This robust well muscled farm working fellow had a deep laceration to his left gastrocnemius some years ago. Also the fibularis tendons had to be repaired.

We have noted that the "wheel" transfer of load from one side to the other has (here) left toe to right heel (POINT to POINT) transfer, a solid indicator that sensation is OK and running this show. The wheel is there, but, mmmmmm... looks a little weak. So, sensory is OK, as the wheel reflects TRUST. Security in transition. Without sensation, things have to bang to confirm stablility before weight is shifted – at all. Here the transfer is just a bit low. Less trust (security) in

HANDLING the load. Once again we see expectation as a guide to walking form. We will look at a few more relationships in this (near recovery) walk. Note neck location just as right "step" happens.

The travel that the body made (c of g or neck is easier by eye) is just under 75% of the radius of the STATURE CIRCLE (diameter = standing height. Radius = center-of-mass to floor). While step lengths may be equal, one sided pathology will make the distance the body goes - for each side's step – different, for example as in "step to" gait. We also note the blue lines. The first was right hip to ankle at right heel strike. The more leftward one is the left hip to ankle line at left heel strike. Looks symmetrical. Good. But the orange arrow head under the right heel is showing a minimal heel rise as left heel

lands. So, there is a wee bit of lack of trust in transfer expectation to the left side. This will become much more obvious on uneven ground where ankle/foot control contouring must time to the forward progression. You have seen enough. What was his main complaint? [ Difficulty shifting gears on his motorcycle – a left ankle foot job] ^ Copy between brackets and paste to text notepad to see the answer - or at very end. BEYOND SKEPTICISM Another trick to eye training is to NOT BELIEVE the diagnosis that comes with the subject. Further, do NOT BELIEVE that that diagnosis – if correct – is what the books or experts tell you it is. See only and all of what is there. Our greatest ever repeating example is 'hemiplegia'. If you see a patient who has the diagnosis of 'left hemiplegia', there is a slight chance all the bodily abnormality is on the left side. It could happen, but it is rare. Childhood hemiplegia causes are quite unlike adult and so effects differ in quality and distribution and of low likelihood to be totally on one side. In fact, many have one sided spastic diplegia. Now spastic diplegia has the typical lower limb crouch spasticity. But that pathology in more severe isn't just more spastic the periventricular distribution widens. That tickles the large nearby nuclei that add a bit of mild dystonic quality to the hands. In adult stroke – middle cerebral artery typically – the worst hit is hand and arm and the knee & foot less so as they go into the anterior cerebral artery zone. Arm worse than leg. Serious sensory loss is most likely. More severe that sensory loss extends to the leg. In children we often see mild hemiplegia with spastic diplegia. No, NOT TRIPLEGIA. Not 3 of a thing. There is hemiplegia quality and

there is spastic diplegia quality. Spastic quadriplegia is a term to avoid altogether. It was taken and copyrighted by spinal injury. Just don't use that term. Widespread anoxia or toxic versions (carbon monoxide etc.) cause TOTAL BODY [favored term goes here... they're all wrong anyway as these are never just spastic -or- dystonic -or- rigid -or- athetoid or...] But, there are bilateral hemiplegia cases – they don't look nor act like total body involvement nor spinal quadriplegia. OK, got that. We have a kid who is called left hemiplegia but he seems to be on toe on BOTH sides. Remember mirroring? Seeking symmetry? When the walking stops does the unexpected on-toe side go down flat? Feels OK when sitting even when that knee is extended? Mirroring. But, you looked and tested and that seems a bit reactive to quick passive dorsiflexion. Oooo, a low grade spastic diplegia trying to sneak by. Under a general anesthesia you will miss this completely. OK. Let's assume we have a hemiplegia. What do we make sure to say we see or say we did not see? Look for the stance leg to bend into swing phase. The thigh flexes to initiate swing. A troublesome plantar flexion makes the swing clearance requirement high and so some side sway and even extra knee flexion might be seen. But, if that knee bends into swing then you only have equinus to fix surgery, casts, AFOs – whichever fits the resistance level. NEVER use AFO to CORRECT plantar flexion stiffness. That will rocker the foot. The midfoot will yield before the plantar-flexion source. If a cast, then only to the arch. No forefoot or same as AFO. Only cast what slack comes with the knee bent. No pressing force at all. We have seen crushed talus with ankle nerve damage from extruded bone.

Hemiplegia

We define three main groups for different treatment needs.

Group 1

The knee bends as the thigh flexes. This is before the foot advances. Some call this (old wrong terminology) preswing. It isn't “pre”. The psoas swings the thigh which then swings the shin. If the knee resists flexing then the foot traps (stubs)

and something else has to clear the stiff swing leg. The well side goes tippy toe and the body leans to the well side lifting the swing side pelvis. Circumduction is actually the exception. It can happen, but don't just say it because 'that is what hemiplegia does'. Easy.

Type two The knee does not bend going into swing. Beware. We know that knee flexion does not normally come from knee flexors. Typically thigh flexion (psoas) is the knee flexor. Not happening as swing is initiated. Must ask WHY ? Two causes for most. If parental nagging got the poor kid's heel down (but the ankle is still plantar-flexed) then bending the knee is nearly impossible due to foot/ankle resistance firmly planted on the ground. This is called 'ground reaction' (Newtonian version of 'reaction', you press the ground which presses back). If it is the ankle/foot then it is a type 2 B. How to know? “Billy, walk on your toes.” “I'm not allowed..” Hey kid, I am the boss here. You can walk on your toes.

OR – apply a cast (toes free to metatarsal heads) with a heel wedge. Knee magically bends going into swing? = 2B , if still stiff, it is 2A 2B is actually type 1 in disguise. So we ask this question when we see a stiff knee in swing phase: “2B or not 2B? THAT is the question.”

A badly pitched AFO will also have you quoting Shakespeare. Regardless of the prescription wording “Well done is better than well said.”

Type 3

Dense hemiplegia. This is closer to adult type and so has similar needs and perils. It is a mix of generalized mass action & sensory impairment. The worst cases can be made to get around quite well unless you fix everything, then they are busted! The bad side becomes simply a crutch. The stiffer it is the more RELIABLE it is.

Actually the entire side is a stick. When that hip is thought to swing, look closer. The good side is swinging the entire bad side. What looks like bad side hip flexion is actually good side extension.

Sticks have no feeling, but they work. The key is that they have zero degrees of freedom. They don't bend. That allows the good side to know where the other foot is. We know where a cane tip is. We can project locality as long as the thing doesn't change.

We saw a woman in consultation because she had lost walking skill after having a total knee replacement. Why the replacement? She had a quite stiff knee. Seriously. No. Really.

And she was telling this from one side of her mouth. The request? Should the knee replacement be revised? Seriously.

But about that stick. If it were a hocky stick you certainly would use it upside down. Otherwise, the stick would pitch back on every ground contact. Same with the foot. Get THAT out of plantar flexion to allow but held stiffly in an AFO such that it plants without a back thrust and not so planted that it can't be tilted forward by progression. Watch facial cues. Does it feel OK? Yes. Does it hurt? Yes. Does it sing Amazing Grace? Yes. Meanwhile the face is gesturing different more appropriate responses and even waving off the vocalized answers. Beware of verbal answers in hemiplegia. Which side is answering?

Mostly we need to do repair in types 1 & 2.

Making a pivot foot for type 3 is about it. Avoid 99% of the stuff that seeks returning or improving motion. Another trap. There may be a wee bit of hemiplegia-like reaction in spastic diplegia and it isn't seen when awash in spastic cross reflexes. You do the right things and see the expected gait improvement – but – hmm it looks like a mild type 2 hemiplegia? Knee not bending into swing. Not ground reaction. ??? When the thigh is fully extended at the end of stance, the rectus femoris gets a tug from the attachment to the anterior inferior spine on the pelvic brim. That tug can trigger a reflex contraction of the rectus femoris (and recruit the quadriceps by reflex spread) just as

the knee needs to bend from thigh swing. Even preop emg won't catch this as it is buried in the co-contraction emg soup. An ethanol RF nerve perineural injection is usually enough, but occasionally the pelvic attachment needs to be 'recessed' (detached from pelvis and buried in with the rest of the proximal quadriceps. Methods vary. Another wrong concept to beware of: “Out of phase”. What is it exactly? When geeks who only read charts see that a muscle has fired here on the x axis, when it should have been there - it is out of phase. That's a timing expression. It is happening WHEN. The question should be WHAT is firing that muscle & why. So a person with supple calf and very normal ankle range including dorsiflexion keeps going on toe and not for any possible compensatory reason (other foot in plantar flexion?). Look at the slow motion video frame by frame and repeatedly the OK foot posture suddenly plantar flexes just as the swinging knee extension gets to a certain point and pow the foot suddenly points down. That isn't a time issue. It is the overly reflexive medial gastrocnemius (the high speed part of the calf complex) getting tugged on over the medial femoral condyle. Recess that proximal attachment off the condyle to the adductor longus long head attachment at the neutral point of the knee axis and that reaction goes away. It does not lengthen. A lengthening would damage power. It wasn't short. This isn't a common diagnosis, but it is extremely illustrative of this phenomenon where ever it is, not just rectus femoris. I It is a major part of arm posturing during walking reacting to arm swing. Enough. Go eat something. We're done here.

Answer to question [ Difficulty shifting gears on his motorcycle – a left ankle/foot job]

Answer to question [ Difficulty shifting gears on his motorcycle – a left ankle/foot job] \

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