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Objective: 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)]., Design: Double-blind, randomized, and placebo (vehicle) controlled trials (n = 7), and nonrandomized, nonblinded trials (n = 2)., Setting: In-patient program at Samaritan Rehabilitation Institute, Phoenix, Arizona, U.S.A., Patients: 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.)., Interventions: i.t. baclofen (50 micrograms) in 1 ml preservative-free normal saline into the L1-2 interspace., Outcome Measures: 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., Results: 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., Conclusions: 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.

When administered systemically to spinalized animals, clonidine, the prototypic alpha 2 adrenergic receptor agonist, purportedly acts at spinal sites to suppress motor responses related to painful peripheral and vesical stimulation and spasticity, and to improve vesicourethral coordination. Hence, the action of clonidine (400 micrograms in three divided doses in a 16-hour span) on spinal vesical and somatic reflexes was examined in five patients with suprasacral spinal cord lesions by assessing volume-induced micturition reflexes and limb motor discharges that occurred spontaneously or were elicited by noxious and nonnoxious cutaneous stimulation. Clonidine caused a significant reduction in (1) blood pressure, (2) amplitude of detrusor contraction, and (3) vesical external urethral sphincter dyssynergia. Limb motor electromyography discharges were not markedly attenuated, although spatiotemporal changes (eg, irradiation, after-discharges) were observed in some of the patients. The results are ascribed to binding to spinal cord alpha 2 adrenergic receptors located on segmental and intersegmental (propriospinal) interneurons, released from descending inhibition, with greater motor system specificity on striated sphincter innervation. Clonidine may be clinically effective in the treatment of hyperactive micturition reflexes in patients with chronic spinal lesions.

This study was designed to determine the rates of gastric emptying of water, saline and a 20% glucose solution in patients with gastric and duodenal ulcers. In all subjects, gastric emptying was fastest after administration of the saline, slower with water and the slowest with glucose. Significant statistical differences (p less than 0.05) in emptying rates between normal subjects and the group with duodenal ulcer were seen when water and saline but not glucose were used. We conclude that inhibitory effects of the osmotic receptors are not changed in gastric and duodenal ulcer patients. However, the emptying rates were higher when osmotic stimulus was withheld.

Ambulatory patients with hemiparesis were given auditory feedback of weight bearing on the involved leg in order to achieve symmetrical standing. A device for augmented sensory feedback, the Limb Load Monitor, was used for the training. Patients who could correct their limb loading pattern during the first treatment session learned to achieve symmetrical standing. Results are also related to the magnitude of weight bearing on the involved limb and the side on which the lesion occurs. These findings suggest that the patients utilized the feedback signal to control an inherent activity.