We have been reminded over and over again in recent weeks how intimately arm swing is tied to leg swing. We have recently had clients in our practices with strokes (ischemic and hemorrhagic), transverse myelitis, inflammatory neurologic disorder and the plethora of biomechanically pain-mediated gait responses affecting the limbs, including the upper limbs which manifest many variations in these people’s normal gait neuro-mechanics.
We are even reminded of the recent triathlete who had a right hip weakness that was allowing him to drift into the right frontal plane in running and biking. Upon asking about further symptoms he mentioned left hand tingling on longer bike training rides. We asked if he recalled sliding/shifting onto the right side of the saddle/seat often to find power in the right leg and he mentioned matter of fact that it is a constant awareness. We then suggested that he was having to over pressure into the left handle grips to keep the bike on a straight line because of the right pelvis-saddle shift. He was wide eyed and shocked that it was what he was in fact aware of. Moral of the story: even in on the bike opposite arm and leg action are intimately tied together. After testing and assessment it was clear that a function TOS (thoracic outlet syndrome) was in effect because of shortness and increased tone in the left pectoral chest wall compromising neurovascular bundle compression and generating hand paresthesias (numbness/tingling). A simple fix if you fix the right pelvic frontal plane drift. If you try to fix the TOS at the shoulder-neck level resistance to progress is likely.
Arm swing is a sneaky thing. There are many variables. We have discussed many of these arm swing variables in 38 previous blog posts (link here) and we have whole lecture here on arm swing (this slide is part of that in depth lecture).
In the pubmed article below there is new research delving into passive and active components of arm swing. There are both, clearly. But what a reader needs to take away is that a clinical examination must be part of every assessment to discover the active components (muscular and neuromuscular) that are missing (ie. weak posterior deltoid, lat dorsi etc) and which need fixing and rehabilitation and the passive components that are inhibitory to the big picture (mobility, stability).
It should be clear by now, if you have been with us for at least the last year, that what you see in someone’s gait is their compensation, not their problem. Addressing resolution measures to change what you see is a path to deepening the compensation or developing others. Arm swing is intimately tied to the lower limbs, and powerfully so to the opposite leg. A deficit in the leg will be expressed in some way in the opposite upper limb, which in turn forces a compensatory change in the opposite upper limb and thus down into the “other” opposite lower limb. One thing affects many. The wrong intervention drives bigger problems, so make sure you know your gait “normal” parameters and be sure a clinical examination is a huge part of your discovery toward the answers for your client.
The results confirm that passive dynamics are partly responsible for armswing during walking. However, without muscle activity, passive swing amplitude and relative phase decrease significantly (both p<0.05), the latter inducing a more in-phase swing pattern of the arms. Therefore, we conclude that muscle activity is needed to increase armswing amplitude and modify relative phase during human walking to obtain an out-phase movement relative to the legs.
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