This client came to see us after a surgical proceedure to remove a dead (osteonecrosis) medial sesamoid under the 1st metatarsal head and a later surgery to fix a progressing hammer toe of the 2nd digit. What we really want you to see is the huge divot/depression under the 2-3 metatarsal heads. Also note the accumulation and relocation of the normal MET head fat pad now located distal to the MET heads. It is as if the fat pad is trying to hitch a ride on the toes now ! This is a case of Metatarsalgia secondary to fat pad displacement (displaced from the divot area to the flexor crease) secondary to surgical sequelae.
What is additionally cool in this case is the fact that this client has an almost complete webbing of the 2-3 toes so many of the normal independent muscular functions are no longer independent. After the surgeries this person presents with tremendous loss of flexor and extensor function of the 2-3 toes. Lumbrical testing was most obviously impaired, completely absent in fact, in these 2-3 toes. On the ground the patient was also unable to achieve any flexion-press of the toes into the ground, he was able to flexion/hammer curl which will obviously put them at risk for hammer toes in the future. But what is important here is that without the ability to PRESS the toes into the ground particularly while in stance phase the lumbricals will not help to hold the fat pad in its normal location under the MET heads. Nor will they be able to to perform their other major functions, namely: thinking from a distal to proximal orientation (a closed chain mode of thinking), they actually plantarflex the metatarsal on the fixed phalynx, assist in dorsiflexion of the ankle, and help to keep the toes from clawing from over recruitment of the flexor digitorum longus.
This client’s MET head pain is obviously caused by lack of cushioning of the head since the fat pad is displaced. There are plenty of other biomechanical abberancies now, the Windlass mechanism will never be the same becuase it is without one of the sesamoids, the hallux short flexor (FHB) is impaired on the medial head without the sesamoid so hallux flexion will become a problem. Do we really want to see such compromise of the medial tripod ? Heck no, we need sesamoid implants ! There is a novel idea ! When a sesamoid is taken out we need to replace it ! Think about it !
There is so much more to this case, but we will stop here. It’s Christmas after all ! This poor lady was told to wish from Santa for a medial sesamoid implant under the tree and a sudden spontaneous activation of the lumbricals to retract the fat pad back under the MET head so as to reduce her pain. Hey, wishing can’t hurt !
Merry Christmas and Happy Holidays to you all gang, whatever your faith we wish you well,
from Shawn and Ivo…… The Gait Guys
(PS: we included below more from the body of the article we wrote long ago called “The Lost Lumbricals”. So for those of you who wish to geek out more on Christmas, read on …
EXCERPTS FROM “THE LOST LUMBRICALS”
The lumbricals of the foot attach proximally to the sides of adjacent tendons of the flexor digitorum longus (with the exception of the 1st, which only attaches to the medial side) and attach distally to the medial aspect of the head of the proximal phalynx and continue on to the extensor hoods in toes 2 through 5. Their typical function is described as flexion of the proximal phalynx and extension of the proximal and distal interphalangeal joints. They have the unique ability to compress the metatarsal-phalangeal and interphalangeal joints. These are “open chain” functions as described, unless you are in the habit of waving to people with your toes, they often are used quite differently in the gait cycle with the foot affixed to the ground.
The lumbricals are most active from midstance to preswing. That means they act predominantly in the closed chain. The lumbricals, along with the other intrinsic muscles of the foot, play a role in maintaining the medial longitudinal arch of the foot. Along with the interossei, they play a role in stabilization of the forefoot during stance phase and rearfoot during preswing. One author has proposed that overpronation is due to a lack of neuromuscular control of the intrinsic foot muscles to stabilize the tarsal and metatarsal bones and therefore modulate the speed of pronation.
Thinking from a distal to proximal orientation (a closed chain mode of thinking), they actually plantarflex the metatarsal on the fixed phalynx, assist in dorsiflexion of the ankle, and help to keep the toes from clawing from over recruitment of the flexor digitorum longus.
Clawing toes during gait, which are considered abnormal, are defined as extension of the metatarsophalangeal articulation, and flexion of the proximal and distal interphalangeal joints result from a foot attempting to stabilize itself during the terminal stance and preswing phases of gait. This is an attempt to help propel the body forward, often accompanied by overactivity of the flexor digitorum longus, tibialis posterior, flexor pollicus longus, and gastroc soleus groups. Overactivity of these groups causes reciprocal inhibition of the long toe extensors and ankle dorsiflexors (tibialis anterior for example), causing the toes to buckle further and a loss of ankle dorsiflexion; in short, diminished ankle rocker.
Now think about the changes in the gait cycle in the above scenario. There will be a resultant shortened step length, diminished ankle rocker, increased forefoot rocker and premature heel rise. This will necessitate an increased extension at the metatarsophalangeal joints, shifting the tendon of the lumbricals upward and behind the transverse metatarsal joint axis, causing even more extension now at this joint. Chronically over time, this causes displacement of the fat pads anteriorly from under the metatarsal heads and is one of the main reasons metatarsal head pain (metatarsalgia). In the past have you made the apparent simple diagnoses of metatarsalgia, shin splints, stress fractures or Morton’s neuroma without knowing a more plausible cause ? Do you now feel you have better answers to these clinical phenomena ?
Now think about changes up the kinetic chain and the potential musculoskeletal implications of muscle inhibition, overfacilitation and joint dysfunction, often with neurological sequelae. With lumbrical dysfunction (weakness) and the resultant lack of ankle dorsiflexion, you have less hip extension. So, you borrow some from the lumbar spine, with increased compressive forces there and an increase in the lordosis, which causes an increase in the thoracic kyphosis and cervical lordosis. We still need to get this leg up and forward to continue our progression ahead, so now we fire our hip flexors instead of the abdominal obliques. And because there needs to be cooperation of the abdominals and hamstrings to maintain pelvis neutrality, this further fuels inhibition of the gluteals thus further compounding the loss of hip extension. Now how about a little increased shoulder flexion on the contralateral side to assist getting that leg forward? Don’t forget that we have altered the thoracic kyphosis and thus changed scapulo humeral mechanics. Now neck/shoulder pain all from bad feet? Maybe. These muscles developed and exist for a good reason, do your best not to dismiss them and their function the next time you see a tortured foot.
When patients have continued dysfunction, consider the base and where it all begins. Consider function in the context of where it occurs. Proper evaluation of the feet and gait can provide valuable clues as to the etiology or manifestation of continued problems. Important? You decide.
The Gait Guys
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