Ivo Waerlop DC DABCN, Shawn Allen DC, DABCO, Robert Lardner PT
When was the last time you thought about the function of your foot’s plantar lumbricals ? How about their role in the gait cycle? When was the last time you actually evaluated them? Are they really that important? Read on and then you decide.
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 (1,2). 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 (3). There is also a small adductory moment to counteract abductory shear, due to the tendon passing medial to the metatarsal-phalangeal joints (4). 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 (5,6). 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 (7). Along with the interossei, they play a role in stabilization of the forefoot during stance phase (8) and rearfoot during preswing (9). Jam (10) proposes 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. When was the last time you watched someone’s toes while they were walking? How about casual observation during your exam?
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 (11) 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 (12,13). 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 (14) (please see our original article at http://www.chiroweb.com/archives/25/23/14.html)
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 (15) 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.
Dr. Ivo Waerlop can be reached by email at : drivo@netzero.com
Dr. Shawn Allen can be reached by email at : doc@doctorallen.com
Robert Larder can be reaced by email at: rlpt@sbcglobal.net
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10. JAM: www.aptei.com/articles/pdf/IntrinsicMuscles.pdf
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14. Waerlop and Allen. Pedographs and Gait Analysis: Clinical Pearls and Case Studies. 2006
15. Bjosen-Moller F, Flagstad KE. Plantar aponeurosis and internal architecture of the ball of the foot. J Anat 1976, 121(3):599-611
