Abstract
This updated white paper argues that carpal tunnel syndrome may be driven not only by mechanical compression of the median nerve, but also by lymphatic stagnation at the distal radial and ulnar collecting junction of the wrist. Within this model, elevated compartmental pressure, intraneural edema, nocturnal worsening, and part of the benefit seen after carpal tunnel release can all be interpreted through impaired lymphatic egress and its downstream neurovascular consequences.

