Clonidine inhibits vesico-sphincter reflexes in patients with chronic spinal lesions.

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.

Antidepressant exacerbation of spasticity.

Patients with spinal cord injury (SCI) may develop depression. This may be related to adjustment to living with an SCI in addition to dealing with complications of the injury, such as spasticity. Pharmacologic treatment of depression can be difficult because of neurochemical and receptor changes that are associated with SCI. Newer antidepressant agents are purported to have selective activity by alteration of serotonergic neurotransmission. A case report is presented that illustrates exacerbation of spasticity by this family of antidepressant medications. Mechanisms possibly explaining this exacerbation of spasticity are the effects of serotonin on motor neuron and reflex activity, denervation supersensitivity, and the serotonin syndrome. Understanding the relationship between serotonergic systems and spasticity can be important in treating depression in patients with spasticity.

The effect of a low dose of intrathecal morphine on impaired micturition reflexes in human subjects with spinal cord lesions.

The potential therapeutic value of a low dose (200-250 micrograms) of intrathecal (i.t.) morphine on bladder capacity was tested in six subjects with chronic suprasacral spinal cord lesions. Micturition reflexes were examined by saline fill cystometry accompanied by EMG recordings from the external anal and urethral sphincters and selected lower limb muscles. Hyperactive detrusor reflexes were associated with a low capacity bladder in five of the six subjects. All subjects revealed vesicoexternal sphincter dyssynergia, and vesical-induced and spontaneous contractions of the abdominal and lower limb musculature. The results was incontinence and frequent catheterizations. Within 5-15 min of the bolus morphine injection into the L1-2 i.t. space, bladder capacity increased to near-maximal values in all subjects. Soon thereafter, uninhibited detrusor contractions, spontaneous motor discharges, and vesicosomatic (limb) reactions were abolished. A peak effect was observed within 2-4 h. Alterations of bladder capacity persisted for 18-22 h. Side effects included pruritus and nausea. Intrathecal morphine acts at sacral spinal cord sites, e.g., primary afferents and/or dorsal horn neurons, mediating vesicovesical and vesicosomatic (sphincter, limb) reflexes, and spontaneous motor discharges. Clinically, i.t. morphine may be an effective therapy for individuals with suprasacral spinal cord lesions when a low capacity bladder interferes with their quality of life.