Case of the Week 6-2-97: What people said...

Hello, this is Dr. Sang-Hyun Cho.

1. What effect has the femoral nerve lesion had?
   The lesion seems to have caused partial weakness on the left knee
extensor muscles (mainly vastus lateralis muscle).   That is because the
femoral nerve supplies all the four muscles of knee extensor and the
left-side EMG record shows relatively insufficient firing of the vastus
lateralis.   Report of her diagnostic EMG & NCV study would give us more
accurate diagnosis.

2. Why does the trunk lean to the right during left stance?
   During the left "loading response period", her weak left knee
extensor was not able to act as normal shock absorber using eccentric
contraction .  You can see it on the "knee flex-ext" plot of the
Kinematics report; the normal "initial flexion wave" has disappeared on
the left side.   In order not to collapse during the initial moment of
left stance phase, she must keep the left knee extended using its
passive extension-lock mechanism.   You can also find its extreme
examples from poliomyelitis victims.   The end result ?   The effective
length of the left leg become longer and pushes the left pelvis
upward.   Then the trunk leans toward right.

3. What is responsible for the abnormal pelvis rotation in the
transverse plane?
   Knee extensor muscle is essential for swinging leg advancement.  
When it is not strong enough, pelvic motion helps swinging leg
advancement; big internal pelvic rotation wave occurs("pelvic-rotaion"
plot of the Kinematic report).

4. Why does the right knee fail to extend fully in mid-stance?
   I think this question may have rather controvertial answers;
sometimes the video observation does not match exactly with its
kinematic report.    When a subject passes the straingt walkway with
his/her pelvis set much internally rotated to either
directions(intentionally or un-intentionally), the "knee flex-ext" plot
will give us somewhat more flexed (elevated) graph.    I have heard that
such phenomenon is due to characteristics of current 3D gait analysis
system hiring surface markers and joint attitude estimation program.  
You can check by yourself if your have such system.  We have done it
already, because we have occasionally encountered CP hemiplegia children
who walk that way and give us strange "knee flex-ext" plots.    I like
to call such patients as "side steppers" or "crab walkers".   Maybe that
could be an interesting topic to discuss about on CGA.
********************************************

Sincerely,
Sang-Hyun Cho

===================
Sang-Hyun Cho MD. Msc. Lecturer
sanghyun@bora.dacom.co.kr
FAX 82-2-363-2795
Yonsei University, College of Medicine, 
Dept. of Rehabilitation Medicine
C.P.O. BOX 8044, Seoul, S-KOREA


Dear Dr. Cho and others,

Thank you for your (second) very comprehensive reply to the Case of the Week. I'm sure everyone has immediately trashed the first - we never even read it! You have rightly highlighted several very interesting topics, which I would like to develop...

>1. What effect has the femoral nerve lesion had?
>   The lesion seems to have caused partial weakness on the left knee
>extensor muscles (mainly vastus lateralis muscle).   That is because the
>femoral nerve supplies all the four muscles of knee extensor and the
>left-side EMG record shows relatively insufficient firing of the vastus
>lateralis.   Report of her diagnostic EMG & NCV study would give us more
>accurate diagnosis.

Here are the EMG & Nerve Conduction Velocities, as requested (please note that I
have - no doubt badly - translated from the German!)...

EMG:
Rectus fem. Left: no spontaneous pathological activity.
Chronic neurogenic motor unit action potentials, prolonged with frequent large amplitude spikes (up to 14 mV!). Maximal contraction resulted in a large amplitude pattern.

Left Vastus med.: no spontaneous pathological activity.
Chronic neurogenic motor unit action potentials, normal response to maximal contraction.

Left iliopsoas: no spontaneous pathological activity, no certain pathology. Long motor unit action potentials. Reduced activation pattern on maximal contraction, 
but patient cooperation was poor. 

Fem. nerve NCVs:              Right      Left
Latency (vastus med.)         4.5 ms    5.5 ms
Amplitude                    17.0 mV    4.6 mV

Summary: old left femoral lesion, distal to the branch to iliopsoas, and chronic neuropathy picture in left vastus medialis with high-grade axon loss.


>
>2. Why does the trunk lean to the right during left stance?
>   During the left "loading response period", her weak left knee
>extensor was not able to act as normal shock absorber using eccentric
>contraction .  

While I agree with this, I do not like the phrase 'Shock absorber'. Although this term
is often used for the loading response, it is strictly incorrect. Shock is the very brief
transient force that occurs at heel strike, which is a function of the visco-elastic properties
of the shoe and foot and can therefore not be prevented or modified in any way by the musculoskeletal system.

You can see it on the "knee flex-ext" plot of the
>Kinematics report; the normal "initial flexion wave" has disappeared on
>the left side.   In order not to collapse during the initial moment of
>left stance phase, she must keep the left knee extended using its
>passive extension-lock mechanism.   You can also find its extreme
>examples from poliomyelitis victims.   The end result ?   The effective
>length of the left leg become longer and pushes the left pelvis
>upward.   Then the trunk leans toward right.

I agree that trunk sway is often seen in polio, but it seems to me that the trunk usually
leans to the side of the pathology during stance phase. Have a look, for example, at
Cases of the Week 14-8-96 and 6-6-96:

/archives/14-8-96

/archives/6-6-96

The latter patient is complicated because she has bilateral involvement, but note that both subjects always leans towards the paretic leg when it is in stance phase. By contrast, this week's case leans to the CONTRALATERAL (right) side when her paretic (left) leg is in stance. This continues to puzzle us, and was the reason I presented her for your
comments.

>
>3. What is responsible for the abnormal pelvis rotation in the
>transverse plane?
>   Knee extensor muscle is essential for swinging leg advancement.  
>When it is not strong enough, pelvic motion helps swinging leg
>advancement; big internal pelvic rotation wave occurs("pelvic-rotaion"
>plot of the Kinematic report).

Sorry, I phrased the question poorly. I am interested in why she leads with the
pathological side, i.e. pelvis & trunk internally rotated on the left.

>
>4. Why does the right knee fail to extend fully in mid-stance?
>   I think this question may have rather controvertial answers;
>sometimes the video observation does not match exactly with its
>kinematic report.    When a subject passes the straingt walkway with
>his/her pelvis set much internally rotated to either
>directions(intentionally or un-intentionally), the "knee flex-ext" plot
>will give us somewhat more flexed (elevated) graph.    I have heard that
>such phenomenon is due to characteristics of current 3D gait analysis
>system hiring surface markers and joint attitude estimation program.  
>You can check by yourself if your have such system.  We have done it
>already, because we have occasionally encountered CP hemiplegia children
>who walk that way and give us strange "knee flex-ext" plots.    I like
>to call such patients as "side steppers" or "crab walkers".   Maybe that
>could be an interesting topic to discuss about on CGA.

Coinicidentally, this point came up last week at the European CAMARN meeting on standardisation, which I attended (explaining the lateness of this reply).

It seems that there can often be varus-valgus artefact in the knee curve due to marker movement or bad positioning. Sandro Fioretti from Ancona also demonstrated large discrepancies in the knee curve (particularly in swing phase) according to which 3D angle convention (Cardan, Euler etc.) is used. This has important implications for us all, since no one convention is 'correct'! Basically, we should take care in interpretting curves when
there is a lot of flexion in the knee joint. Of course, CP diplegics often walk with quite 
flexed knees, so this is quite worrying. I'd be very happy if someone who understands this problem better could further enlighten (reassure) us!

Best wishes,

Chris


Chris et al

Sorry this has taken so long but a week sunning myself in Italy, a week
struggling to download data over a dodgy www connection and a week finding
an hour to mull over the problem in the bath have all contributed to the
delay. Let's call it case of the month?

I think the overall answer to your questions is fairly straightforward in
that this is the gait pattern that a person with compromised knee extensor
function adopts if they wish to preserve a reasonable step length on the
affected side.

In order to stabilise the knee the ground reaction vector must pass in front
of the knee generally requiring the centre of mass to be anterior to the
knee (with a little tolerance for inertial effects). In the "polio" gait
referred to this is acheived by leading with the sound side and using a
short step length on the affected side and anterior tilt of pelvis and trunk
to move the centre of mass forward stabilising the knee. Because of the
pelvic rotation and the anterior tilt this gives the impression of lean to
the affected side (there may be some true lean in this direction as well).

Our patient however wants to get a good step length on the affected side and
in order to stabilise the knee must push the centre of mass as far forward
as possible over the affected foot in early stance. A consequence of doing
this is that the centre of mass is transferred more laterally than normal
and this is observed as the reduced hip abduction moment. The knee moment
shows that stabiltiy has been achieved. Interestingly the hip moment is
fairly normal showing that shift of centre of mass is acheived by moving
pelvis and trunk together as opposed to the "polio" gait in which it
achieved by pelvic and trunk anterior tilt and in which the hip extension
moment is increased in early stance. This also explains why she leads with
the affected side - to keep the centre of mass as far forward as possible.

The main issue for her having achieved this knee stability by
anterio-lateral transfer of weight is how to get the wight back medially. In
able bodied gait the centre of mass is always well within the base of gait
and gravity simply pulls it back in. However her centre of mass is lateral
and requires some help so she combines anterior tilt with an interiorly
rotated pelvis, pelvic tilt and true lateral trunk flexion to the opposite
side to ensure that her centre of mass keeps forward but also begins to move
back medially. Effectively she is always leaning to the right to make sure
she doesn't fall over to the left. Of course the best way to maintain  this
gait is to flex the sound limb so that it is always slightly lower than the
affected one (see pelvic tilt, knee, hip and ankle flexion).

Having introduced such a pronounced lateral shift and then working hard to
regain the medial shift she then requires to arrest this as she accepts
weight on the sound limb. We can see the burst of power absorbtion at the
sound knee which is her arresting her fall onto it. The other factor which
is important is the marked internal rotation of the right hip.  This ensures
that although the pelvis is externally rotated (viewed from the right now)
the right leg is actually internally rotated with respect to the line of
progression (this is clear form the foot progression angle) and that the
forces generated by this limb have a medially directed component. This is
required so that in terminal stance not only is the sound limb pushing
forward but also medially, pushing the centre of mass forward and over onto
the affected limb. Which is back to where I started this description of the
gait cycle I think.

The low down of this is probably that there is little we can do for this
patient. She seems to me to be optimising her available resources to acheive
what is at 1.31 m/s probably quite a functional gait if a little high in
energy consumption. I can't see anything we could do to assist her.


Additional points:

1) I don't think we have a problem with projection of Knee flexion onto knee
varus/valgus here. If this is the case then the pattern on the varus/valgus
graph is generally quite similar to the pattern of knee flexion. This is
possibly the case on the left (albeit inverted) but certainly not the case
on the right. The blip of kneee varus in mid-swing is a little odd.
Interestingly it occurs at the same time as a blip of external rotation in
the foot progression.

2) Can we please stop referring to pelvic rotation as either internal or
external. It doesn't help at all in discussing a case like this to have to
remember which side we are looking at when talking about the pelvis. Any
suggestions?

3) It does not come out from the data presented but this girl would almost
certainly show increased excursion of the centre of mass in both the
vertical and medio-lateral directions, high energy consumption as a
consequence, and exagerrated components of the ground reaction, particularly
the medio-lateral components. 


Is it too late for anyone to summon up any energy to feedback on this?

Richard Baker
Gait Analysis Service Manager
Musgrave Park Hospital
Belfast
Regarding the points for discussion on the girl with femoral nerve palsy.  We can up with the following explanation:  While in left
stance, the girl wants to shift her center of mass (COM) away from her left leg (the affected limb) towards the right. To achieve
this the girl hikes her left hip, moving the COM to the right. To walk the girl compensates by swinging her left leg around. This 
process causes the pelvis to rotate anteriorly and to the right in a clockwise direction.   Do you concur? clif monteith, LPT 

Clifton Monteith <clifton@dnet.net> 

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