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The Relational Inhibition Myth

The Relational Inhibition Myth

Seems many are having difficulty grasping this concept and with good reason. Its a Myth.

IF you are doing “muscle” to “muscle” testing (which I consider the lowest on the totem pole of AK) Then you will be confused, frustrated an chasing your tail.

The fact that you found 23 muscles to one dysfunction should have been your first clue that the relational inhibition in GLOBAL. There are No relational patterns

Now, If you Choose to use Relational Inhibition as an indicator thats a different story. This would be where you test a “movement” under a specific directional load to challenge the movement. Then you can use ANY indicator “muscle” test to determine if the Joint could handle the load placed upon it. That is ALL you are testing- can the joint handle the load.

For example if I am testing internal rotation of Humerus in forward flexion, elbow both at around 85 degrees (Like Arm wrestling) and I resist just the internal rotation of the shoulder, then I can Test whatever indicator muscle that was strong in the clear. If the “Muscle” test “fails” it tells you the Joint is dysfunctional under that particular directional load. However, is NOT telling you where the dysfunction is located :)

Some Science research to back it up If you care to read it

Spinal inhibition of descending command to soleus motoneurons is removed prior to dorsiflexion.

Geertsen SS1, van de Ruit M, Grey MJ, Nielsen JB.

Author information


It has recently been demonstrated that soleus motor-evoked potentials (MEPs) are facilitated prior to the onset of dorsiflexion. The purpose of this study was to examine if this could be explained by removal of spinal inhibition of the descending command to soleus motoneurons. To test this, we investigated how afferent inputs from the tibialis anterior muscle modulate the corticospinal activation of soleus spinal motoneurons at rest, during static contraction and prior to movement. MEPs activated by transcranial magnetic stimulation (TMS) and Hoffmann reflexes (H-reflexes), activated by electrical stimulation of the posterior tibial nerve (PTN), were conditioned by prior stimulation of the common peroneal nerve (CPN) at a variety of conditioning-test (CT) intervals. MEPs in the precontracted soleus muscle were inhibited when the TMS pulse was preceded by CPN stimulation with a CT interval of 35 ms, and they were facilitated for CT intervals of 50-55 ms. A similar inhibition of the soleus H-reflex was not observed. To investigate which descending pathways might be responsible for the afferent-evoked inhibition and facilitation, we examined the effect of CPN stimulation on short-latency facilitation (SLF) and long-latency facilitation (LLF) of the soleus H-reflex induced by a subthreshold TMS pulse at different CT intervals. SLF is known to reflect the excitability of the fastest conducting, corticomotoneuronal cells whereas LLF is believed to be caused by more indirect descending pathways. At CT intervals of 40-45 ms, the LLF was significantly more inhibited compared to the SLF when taking the effect on the H-reflex into account. Finally, we investigated how the CPN-induced inhibition and facilitation of the soleus MEP were modulated prior to dorsiflexion. Whereas the late facilitation (CT interval: 55 ms) was similar prior to dorsiflexion and at rest, no inhibition could be evoked at the earlier latency (CT interval: 35 ms) prior to onset of dorsiflexion. The observation that the CPN-induced inhibition of soleus MEPs disappears prior to onset of dorsiflexion may explain why soleus MEPs are facilitated prior to onset of dorsiflexion contraction. A possible mechanism involves the removal of inhibition of the descending command to the motoneurons at a spinal interneuronal level because the inhibition was seen in LLF and not in SLF, and the MEP inhibition was not observed in the H-reflex. The data illustrate that spinal interneuronal pathways modify descending commands to human spinal motoneurons and influence the size of MEPs elicited by TMS.



[PubMed - indexed for MEDLINE]

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