Median nerve and Ulnar nerve lesions

Hi all,
I am still a student and have been struggling to understand something in Median and Ulnar nerve injuries.

I understand the reason for the 'Ulnar Claw' being the combination of the loss of innervation to the medial two lumbricals and then the activity of the forearm flexors causing hyperextension of the MCP joint and flexion at the IP joint of the 4th and 5th fingers. It also makes sense to me how a more proximal Ulnar nerve injury (e.g. at the elbow) will make the 'Ulnar Claw' less obvious as there is decreased flexion at the IP joints due to loss of innervation to the Flexor Digitorium Superficialis. This being referred to as the Ulnar Paradox.

Where I get confused is, would't this be the same for the Median Nerve? Why isnt there also a 'Median Nerve Paradox'? The Median Nerve also innervates the Flexor Digitorium Superficialis and the lateral two lumbricals so why wouldnt a distal lesion in comparison to a proximal lesion cause the same 'paradox'? Everywhere where I have looked and also in my varsity notes there is no mention of a Median nerve paradox.

Any help will be really appreciated!!
Thank you,
Caroline

Hi Caroline,
Not sure I understand you question exactly - but does this help?
- Yes, ulnar nerve innervates 2 lumbricals on the ulnar side - but an ulnar claw primarily occurs because the interossei have been paralysed. Remember that each finger has 3 muscles that primarily control MCP flexion - one lumbrical, a palmar interossei and a dorsal interossei. In an ulnar claw all 4 fingers claw - the ring and little finger most obviously because they lose all 3 muscles, but index and middle fingers will also have at least a 'latent' claw (you may only 'see' it in a power grip) because they also lose 2 (interossei) out of the 3 muscles that control MCP flexion.
In an ulnar claw the MCP hyperextension is due to unopposed extension force of EDC and the extensor mechanisms on the MCPs. All that force 'stops' at the MCPs, and the lumbricals are no longer contributing via the lateral bands to get PIP extension.
In a median nerve injury there is paralysis of index and middle finger lumbricals - but you never see overt clawing of these fingers unless ulnar nerve is also paralysedbbecause index & middle finger still have functioning interossei to control MCP flexion. Median paralysis most obviously affects palmar abduction / opposition / flexion function of the thumb. This remains obvious even in a high lesion that involves FPL - only difference may be overpronounced IP flexion in a distal lesion as FPL tries to flex/oppose/palmarly abduct the thumb, but doesn't have help to successfully do so at the first MCP joint. Obviously there is no IP flexion in a high (proximal) lesion.
So - don't forget the interossei! I think understanding their function might be key to your question about paradoxes.
Hope some of that makes sense. Does it help answer your question?
Anne

Hi Anne,
Thank you so much for your help! You did answer my question and were also right about the functoning of the interossei being the reason for my confusion. I originally thought that the interossei were only involved in finger ab- and adduction. After reading your answer I read up a bit more and saw that the interossei do assist the lumbricals in MCP flexion and IP extension! It all makes sense to me now :)
Really appreciate your help,
Caroline