Intrathecal baclofen suppresses central pain in patients with spinal lesions. A pilot study

To assess the efficacy of acute intrathecal (i.t.) baclofen on chronic, dysesthetic, and spasm-related pain (SRP) among patients with spinal spasticity [i.e., multiple sclerosis (MS), spinal cord injury (SCI), transverse myelitis (TMy)].

Double-blind, randomized, and placebo (vehicle) controlled trials (n = 7), and nonrandomized, nonblinded trials (n = 2).

In-patient program at Samaritan Rehabilitation Institute, Phoenix, Arizona, U.S.A.

MS (n = 4), spinal cord compression (n = 1), and TMy (n = 2) in the double-blind trial, and SCI (n = 2) in the nonblinded trial; all had chronic spinal lesions and function-limiting spasticity refractory to oral medications, including baclofen (p.o.).

i.t. baclofen (50 micrograms) in 1 ml preservative-free normal saline into the L1-2 interspace.

Electromyographic (EMG) activity; intravesical and intraurethral pressures; Ashworth Scale and tendon response values; visual analog scales for describing dysesthetic pain intensity; and threshold/EMG relationships after controlled pinch as an indication of nociceptive pain.

i.t. baclofen (a) caused marked reduction of segmental reflexes before suppression of intersegmental reflexes; (b) significantly suppressed dysesthetic pain and SRP with temporal dissociation; and (3) did not influence pinch-induced and musculoskeletal (low back) pain.

The suppressive action of i.t. baclofen on spontaneous and evoked (allodynia) dysesthetic pain suggests that a dysfunctional spinal gamma-aminobutyric acidB receptor system, including functional supersensitivity, is associated with the phenomenon of central pain among patients with spinal lesions. Temporal dissociation regarding the action on dysesthetic pain and SRP suggests that disparate central mechanisms subserve the two clinical states.