What does progressive weakness of the posterior compartment look like?

Look at this video carefully and what do you notice? Can you see the progressive dip in the left heel as time goes on while toe walking? This is a cardinal sign of lack of endurance in the posterior compartment, in this patient’s case tibialis posterior. Your differential, in addition to lack of type one muscle fibers, insufficient vascularity or mitochondria for whatever reason would be circulatory problems as well as conditions causing progressive motor weakness like myasthenia gravis.

Fatigue testing is very important because a lot of times the problem doesn’t come out till the person reaches say a half an hour, an hour or sometimes even many miles into the run or ride. Our job as clinicians is to try to diagnose the problem to the best of our abilities. Our job also is to “exploit their weaknesses” rather than “extol their virtues”. 

If you’re getting somebody with posterior calf pain or a foot drop, or maybe somebody who gets worse over time, consider fatigue testing.

The Tib Posterior...Revisited...

Posterior tibialis tendinitis is a primary soft tissue tendinopathy of the posterior tibialis that leads to altered foot biomechanics. Although the natural history of posterior tibialis tendon dysfunction is not fully known, it has mostly been agreed that it is a progressive disorder.(1)

The tibialis posterior originates from the proximal posterior tibia and fibula and interosseous membrane; it is deep in the posterior compartment of the leg and changes its line of pull from the vertical to horizontal at the medial malleolus. The musculotendinous junction is in the distal third of the leg and the tendinous portion turns 90 degrees at the medial malleolus. It has a broad insertion into the plantar surface of the midfoot, largely into the navicular tuberosity with branches to the sustentaculum tali, and the remainder inserting into the entire plantar midfoot except for the 5th metatarsal(1-3).

 The tibialis posterior (TP) is one of the more important extrinsic arch stabilizing muscles. It is a stance phase muscle that fires from the loading response through terminal stance, acts eccentrically to loading response to mid stance to slow pronation and concentrically from mid stance to terminal stance to assist in supination.(4) Its recruitment seems to be increased with slower walking speeds (5).

Since the foot is usually planted when it fires, we must look at its closed chain function (how it functions when the foot/insertion is fixed on the ground), which is predominantly maintenance of the medial longitudinal arch, with minor contributions to the transverse metatarsal and lateral longitudinal arches (6) ; flexion and adduction of the tarsal’s and metatarsals and eccentric slowing of anterior translation of the tibia during ankle rocker. It is also an external rotator of the lower leg and is the prime muscle which decelerates internal rotation of the tibia and pronation. As the origin and insertion are concentrically brought towards each other during early passive heel lift it becomes a powerful plantarflexor and inverter of the rearfoot.  There is also a  component of ankle stabilization via posterior compression of the tarsal’s and adduction of the tibia and fibula.

Alas, there is much more than the typical open chain functions of plantar flexion, adduction and inversion. Perhaps it is some of these other, closed chain functions, that cause the “progressive nature of posterior tibial tendon dysfunction"(7)?

This muscle is easily accessed through the posterior compartment, lying deep in the midline to the gastroc and soleus (8,9). Care should be taken to avoid the sural nerve, often found between the heads of the gastroc and becoming superficial (and palpable) in the midline where it exits from the inferior junction of the 2 heads of the gastroc (10). The posterior tibial artery, vein and nerve lie on top of the tibialis posterior for the upper 2/3 of its route through the calf, becoming superficial (and palpable) in the distal 1/3 of the lower leg (11). I find starting laterally or medially and angling your fingers, instrument or the needle medially or laterally seems to work best. Make sure to count your layers!

1. Ling SK, Lui TH. Posterior Tibial Tendon Dysfunction: An Overview.  Open Orthop J. 2017 Jul 31;11:714-723. doi: 10.2174/1874325001711010714. eCollection 2017. link to free full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5620404/

2. Blake R.L., Anderson K., Ferguson H. Posterior tibial tendinitis. A literature review with case reports. J. Am. Podiatr. Med. Assoc. 1994;84(3):141–149. doi: 10.7547/87507315-84-3-141. [PubMed] [Cross Ref]

3. Supple K.M., Hanft J.R., Murphy B.J., Janecki C.J., Kogler G.F. Posterior tibial tendon dysfunction. Semin. Arthritis Rheum. 1992;22(2):106–113. doi: 10.1016/0049-0172(92)90004-W. [PubMed] [Cross Ref]

4. Semple R, Murley GS, Woodburn J, Turner DE. Tibialis posterior in health and disease: a review of structure and function with specific reference to electromyographic studies. Journal of Foot and Ankle Research. 2009;2:24. doi:10.1186/1757-1146-2-24.

link to free full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2739849

5. Murley GS1, Menz HB2, Landorf KB2.  Electromyographic patterns of tibialis posterior and related muscles when walking at different speeds. Gait Posture 2014 Apr;39(4):1080-5. doi: 10.1016/j.gaitpost.2014.01.018. Epub 2014 Feb

6. Kaye RA1, Jahss MH.  Tibialis posterior: a review of anatomy and biomechanics in relation to support of the medial longitudinal arch. Foot Ankle. 1991 Feb;11(4):244-7.

7. Rabbito M, Pohl MB, Humble N, Ferber R. Biomechanical and Clinical Factors Related to Stage I Posterior Tibial Tendon Dysfunction.  J Orthop Sports Phys Ther, Epub 12 July  2011.doi:10.2519/jospt.2011.3545.

 8. Howitt S, Jung S, Hammonds N. Conservative treatment of a tibias posterior strain in a novice triathlete: a case report. J Can Chiropr Assoc. 2009 Mar;53(1):23-31.   link to free full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652628/

9.   Lou XF, Yang XD, Jiang SH, Sun CY, Zhang RF.[Study on angle and depth of needle insertion in acupuncture at Zusanli (ST 36)]. Zhongguo Zhen Jiu. 2006 Jul;26(7):483-6

10. https://functionalanatomyblog.com/2009/11/26/the-sural-nerve-anatomy-and-entrapment/

11. Enrique Ginzburg, ... Norman M. Rich VASCULAR ANATOMY OF THE EXTREMITIES in Current Therapy of Trauma and Surgical Critical Care, Mosby; Pages 467–472 2008

A Serious Gait Problem: Pancompartmental Compromise of the Lower Leg.

“Pan” is a prefix (combining form) meaning all, entire, everything, everywhere 

This was a case we discussed during a more recent podcast, perhaps pod 63 or 64? This doctor had fallen asleep with the left leg dangling over the side of his bed. The issue was that the leg not only dangled over the mattress, but also over a wooded side bed frame, so there was a firm upward compression into the posterior/popliteal compartment. He awoke the next day with complete loss of function of the foot and ankle.  This video is 8 weeks after the compressive event and there has been a significant improvement in function, but there are still some deficits here.  Can you see them ?  We will show you come other video clips in a future blog post discussing some other components of his gait but lets get you familiar with the case today.

What you should see here:

1- Left heel shows a staggered drop. He cannot hold heel rise because of compromise to the posterior compartment strength (gastrocsoleus complex). This was a drastic improvement from his complete inability to heel rise at all at on his initial visit. You can easily see the fatiguability of the calf after just a few steps. 

2- There is a pathetic attempt at heel walking; gross function testing of the anterior compartment. What appears to be an attempt at just right heel walking is actually an attempt to do it on both sides, there is just still so much weakness in the left anterior compartment that you cannot even see his attempts to dorsiflex the foot/ankle or toes. But, what we do not show here is that he has non-weight bearing dorsiflexion now, which was completely absent for the first 6 weeks.  

Neuronal regeneration is possible. It takes time.  Depending on your referenced source the numbers vary. But in his case, in 8 weeks there is progressive improvements and he can say for certain that in the last 2 weeks they are exponential.  The time to restoration of neuronal function is said to be directly proportional to the measurable length of nerve damage.  

What is interesting in this case, is that there is anterior and posterior compartment neurologic compromise. This was a case of vascular and mechanical compression to the neurovascular bundle at the popliteal/knee level. 

Wallerian degeneration is a process that results when a nerve is severely damaged. The axon of the nerve which is separated from the neuron cell body degenerates distal to the injury. The part of the axon distal to the injury begins its degeneration within 24-36 hours of the lesioning event and is followed by myelin sheath degradation. Somewhere around 4 days from the time of the injury, the distal end of the portion of the nerve fiber proximal to the lesion begins sprouting in an attempt to regrow and fill the gap along the length of axonal damage. Sources vary, but many seem to indicate a 1mm per day reinnervation. 

More on this case next time, but the stage has been set.

Shawn and Ivo