Case of the Week 01-03-98: What people said...

As I mentioned previously, this one is perhaps the most severe and complex so far. Velocity is very low, at 0.7 m/s. Stride Length only 0.75 m, with a normal cadence. So the problem (as usual) is inadequate stride length.

What is limiting stride length? There are two main possibilities:

Let's look at the evidence for both. Certainly, hip extension is severely limited on both sides. Ankle push-off power is not really too bad (though note the double bump suggestive of ankle clonus (especially right). However, where is it going? If you look at the frontal plane movie, you'll see she has severe lever arm dysfunction on the right, because of toeing-in. Thus, much of the power being generated by this ankle is not propelling the leg forwards.

What's causing the toeing in? Here the physical exam helps: femoral anteversion both left (60°) and right (75°). So why is the right side more toed-in? The hip must be internally rotated too. The kinematics shows an extra 20° on that side. Both frontal hip powers suggest weak hip abductors (Trendelenberg), made worse by the hip adduction, and the reason why she uses her arms so much.

This leaves us with the knees, which are both fixed. Why? It doesn't seem to be rectus/hamstrings spasticity, or at least there's not much EMG evidence (if I read it correctly). Although there are marked rectus signs bilaterally, the hamstrings are less tight. The missing tight knee flexors are, of course, the spastic adductors, which we don't have EMG data on. By the way, the huge knee moments (with consequently severe bone-on-bone forces) are surely going to damage her knees in time.

How is she advancing then? look at the sagittal hip powers - they're huge: on the right both H1 and H3, on the left the pull-off only (H3). There are also big K2s, especially right, but I don't know whether these are artefactual (Cardan angle problem) due to the knee being flexed.

Well, I'm now as exhausted as she must be! I'll leave the treatment to someone else...

Chris

Dr. Chris Kirtley (Kwok Kei Chi) MD PhD Assistant Professor Department of Rehabilitation Sciences The Hong Kong Polytechnic University <kirtley@cua.edu> 


Dear All:
     I hope I'm not to late to comment on this case.  It does look very complex and challenging.
     First I don't understand the idiopathic part of the patient's diagnosis. If premature birth did not occur, was there a perinatal problem or IVH noted.  Our neurologist often notes that 30% of all CP is not associated with prematurity.  My limited experience would suggest that 10% is not associated with premature birth.  Still my point is that we know enough about the pathology.
     The patient has obvious internal hip rotation which appears due mainly to femoral anteversion.  The adductors also contribute to what would appears like scissoring if enough hip motion occurred to allow crossing of the knees. Since hip motion is so restricted it appears as if the knee are tied together.
     From the physical exam I'd suspect the left hamstring of being excessively tight and contributing to the flexed knees; the right may be as well but not as much.  Weakness is a concern for this patient and may contribute to their crouch.
     There needs to be some assessment of hip flexion contractures, such as a Thomas test to determine this contribution.  I'd also like to know about contractures at the knees and ankles.  Looking at the kinematics the ankles appear in dorsiflexion, the right more so than the left, but perhaps this is compounded by midfoot break.
     I agree with the Trendelenburg notion, that lateral trunk shift has a major effect on the coronal moments.
     I don't think that an early plantarflexor moment can be attributed to clonus.  With both ankles in dorsiflexion, it is likely that the early plantarflexor moment is due to knee flexion.
     My surgical recommendations would be bilateral psoas over the brim (assuming there would be hip flexion contractures on physical exam), derotational osteotomies of the femora, bilateral adductor lengthenings and possible bilateral hamstring lengthenings depending on popliteal angles on the table and/or capsular releases if knee flexion contractures were present (which Isuspect but who knows).
     One could approach the derotational osteotomies and psoas lengthenings at the same time by doing intertrochanteric osteotomies.  We have found on some patients that the insertion of the psoas is posterior in these patients and by correcting their femoral anteversion a psaos lengthening is also achieved.  Dr. Chung in Seoul, South Korea, has quite a series of these patients with good results.  If there is still hip flexion contractures at metal out one year later he may elect to lengthen the psoas then.  Perhaps he could comment on this.
    We need a lot more information about this patient to truly make sound surgical recommendations.  Here is what we include on a patient:

HISTORY:
PREVIOUS SURGERIES:
REASON FOR REFERRAL:
CONDITIONS TESTED:
PHYSICAL EXAM
*PASSIVE ROM:   *JBJS, V 77-A, No. 5, pp784-798, 1995.
                                                                      RIGHT           LEFT
HIP     S       EXT-0-FLEX
           C       ABD-0-ADD
           T       ABD (90 HIP FL)
           T       EXT ROT-0-INT ROT (Prone)
 
KNEE    S       EXT-0-FLEX
 
FLEXIBILITY
PRONE KNEE FLEXION (grab)

                ELY
                STRAIGHT LEG RAISE
                KNEE EXT W/HIP @ 90 (grab)
 
ANKLE   S       DORSI-0-PLANTAR
                W/KNEE FLEX
 
FOOT POSITION (weight-bearing)
THIGH-FOOT ANGLE RANGE EXT-0-INT (resting)
TRANSMALLEOLAR AXIS

Trendelenburg:               Leg Length
Equil:  sitting standing     Calf Girth
        Active Dorsi to

Ataxia                         Athetosis
Clonus of Gastroc       Post Tib

 
MUSCLE TONE:  Note velocity-dependent increase in resistance to passive motion.  Test patient supine,
                                 head in mid-line.

                           RIGHT         LEFT
Adductors
Quads
Hamstrings
Gastroc

Scale for grading spasticity (modified Ashworth and Bohannon)
5 = Extreme      Affected part rigid in flexion or extension.
4 = Severe        Considerable increase in tone, passive movement is difficult.
3 = Moderate    More marked increase in tone through most of range of motion but affected part is easily
                        moved.
2 = Mild            Slight increase in tone "catch" in limb movement or mild resistance to movement through
                        less than half of the range.
1 = Normal       No increase in muscle tone.
0 = Hypotonic   Less than normal muscle tone, floppy.
 

MANUAL MUSCLE TEST
Hip     flexion (R/L)
          extension
          abduction
          adduction
Knee    flexion
            extension
Ankle   dorsiflexion
            plantar flexion
            inversion
            eversion
Toe     extension
           flexion
 

(P) = Resistance is given in the patient's active range but active range of motion is less than passive range.
*Plantarflexion grade indicates number of toe rises possible with (P) for partial rise.

Key - Kendall
100%    5       N       Normal: Completes arc of motion against gravity with a maximum resistance.
80%      4       G       Good: Completes arc of motion against gravity with a moderate amount of
                                        resistance or is unable to complete arc of motion when done with a
                                        maximum amount of resistance.
50%     3       F         Fair: Completes arc of motion against gravity.  (3+ takes a minimum
                                      amount of resistance)
20%     2       P         Poor: Moves through partial arc of motion with gravity eliminated.
5%       1       T         Trace: A contraction is felt, but there is no apparent movement of part.
            0       0          Zero: No contraction felt in muscle.

GAIT LABORATORY EVALUATION FORM
Shriners Hospital for children
Portland, Oregon USA         7/93
---------------------- 
Michael Orendurff, MS
Gait Lab
Portland Shriners Hospital
MSO@shcc.org  

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