Article

In patients with Charcot spine, a loss of normal feedback response from the
insensate spine results in spinal neuropathy. Increasing deformity, which can
manifest as sitting imbalance, crepitus, or increased back pain, can result. We
present the case of a patient with a high-thoracic spinal cord injury (SCI) who
subsequently developed a Charcot joint at the T10-11 level that resulted in a
dramatic increase in previously controlled spasticity after fracture of an
existing baclofen catheter. The 68-year-old man with T4 paraplegia presented with
increasing baclofen requirements and radiographic evidence of fracture of the
intrathecal baclofen catheter with an associated Charcot joint with extensive
bony destruction. The neuropathic spinal arthropathy caused mechanical baclofen
catheter malfunction and resulting increased spasticity. The patient was found to
have transected both his spinal cord and the baclofen catheter. Treatment
consisted of removal of the catheter and stabilization with long-segment
instrumentation and fusion from T6 to L2. Follow-up radiographs obtained a year
and a half after surgery showed no evidence of hardware failure or significant
malalignment. The patient has experienced resolution of symptoms and does not
require oral or intrathecal baclofen. This is the only reported case of a Charcot
spine causing intrathecal catheter fracture, leading to increased spasticity.
This noteworthy case suggests that late spinal instability should be considered
in the setting of SCI and increased spasticity.
CI - Copyright (c) 2015 American Congress of Rehabilitation Medicine. Published by
Elsevier Inc. All rights reserved.

Langue : ANGLAIS