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Abstracts of the 8th Meeting of the Italian Peripheral Nerve Study Group: 9
Author(s) -
Vinci P,
Perelli SL,
Martini D
Publication year - 2003
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1046/j.1529-8027.2003.00009.x
Subject(s) - heel , medicine , achilles tendon , deformity , pes cavus , foot (prosody) , physical medicine and rehabilitation , foot deformity , anatomy , physical therapy , tendon , surgery , complication , linguistics , philosophy
Charcot‐Marie‐Tooth disease (CMT) is a genetic neuropathy characterized by a length‐dependent degeneration of motor and sensory nerve fibers. Whereas all authors agree that weakening starts from the intrinsic foot muscles, there is still controversy whether the tibialis anterior muscle (TA) is weak or not in the early stages of the disease. To know this could be important either to understand how the cavus deformity develops or, consequently, to adopt surgical (tendon transfers) and conservative (orthotics, physiotherapy) strategies for prevention or early correction. We measured the power of TA in 110 feet of 62 patients (41 CMT1A, 1 CMT1B, 9 CMT1 without genetic evaluation, 5 CMTX, and 6 CMT2) fitting in the first two stages of the functional classification proposed by Vinci and Perelli. Thirty‐one feet were at stage 1 (forefootdrop or mild footdrop: leg‐sole angle >90< = 100) and 79 at stage 2 (same as stage 1 plus foot rotation on the longitudinal axis: heel angle <0 or >10). Muscle strength was measured by the manual muscle testing and scores according to the Medical Research Council scale. TA power graded 5/5 in 87 (79.1%) feet, 4/5 in 17 (15.5%) and 2/5 in 6 (5.4%). TA was strong (MRC 4/5 and 5/5) in the large majority (94.6%) of the feet in the two earlier stages of the disease. Interestingly, the 6 patients with weaker TA had CMT2. These results support our hypothesis that, in the earliest phase of CMT, foot rotation is due to a stronger and hyperactivated TA, which compensates the footdrop caused by the deficit of the metatarsophalangeal joint stabilization and, in many cases, is not balanced by the weak peroneal muscles.