Baclofen versus diazepam for the treatment of spasticity and long-term follow-up of baclofen therapy.

Baclofen (25 to 60 mg per day) and diazepam (10 to 40 mg per day) were evaluated for spasticity reduction in a double-blind, crossover study in 13 patients over a period of 19 weeks. Both drugs produced overall improvement and there was no significant difference in preference for one or other treatment. Side-effects, especially excessive daytime sedation, were more common in the diazepam group. In a companion baclofen long-term study, 18 spastic patients were treated with baclofen for an average of 4 years. Baclofen discontinuation in this group resulted in a worsening of spastic signs and symptoms in 16 patients, with no evidence of drug tolerance even after many years of baclofen therapy.

Baclofen. Its effect on seizure frequency.

Baclofen has been reported to be epileptogenic in man, but many animal studies have demonstrated an anticonvulsant effect. In 12 patients with a history of epilepsy, baclofen was given in the conventional dosage range. In the six patients with anticonvulsant-controlled seizures, none had a seizure during baclofen therapy. In the six patients with uncontrolled epilepsy, two patients had one more seizure per month while receiving baclofen, and a third went from four seizures per month to one per month. Baclofen does not appear to have a deleterious effect in patients with epilepsy.

Pharmacological rebound: a tool in the evaluation of antispasticity drugs.

Twelve spastic patients with traumatic transverse myelopathies participated in a two-stage, double-blind crossover study using BA-34647 (a new experimental antispasticity drug by Ciba-Geigy) and placebo. Clinical measurements of spasticity were performed before, during and after each stage. Six patients had excellent results receiving a regimen of BA-34647 but not when receiving placebo. Four patients had fair-to-good results with both BA-34647 and placebo. One patient had no significant changes when receiving either drug or placebo, the effective dose not being reached due to excessive body weight. One patient had a shortened trial due to pain and diminished function caused by excessive spasticity. Abrupt changes in post-treatment symptomatology (increase in spasticity) occurred in all six patients who demonstrated excellent results and in all four patients with fair-to-good results. In each of these cases, the increase followed the discontinuation of BA-34647. In no case was there an increase of spasticity following discontinuation of placebo. The effectiveness of an antispasticity drug may be too subtle to be perceived subjectively and objectively. The rebound phenomenon is evidence that a pharmacodynamic effect, though minor, was present.

Bladder training: its role in evaluating the effect of an antispasticity drug on voiding in patients with neurogenic bladder.

Fourteen patients with spinal cord damage were treated with Ba-34647 (Lioresal, Ciba-Geigy), a new antispasticity drug. The treatment was initiated for excessive skeletal muscle spasticity and voiding difficulty. Seven of the patients had been wearing indwelling catheters and seven were catheter-free. The former were given trials at voiding after removal of catheters; the usual assistive methods common to most bladder training regimens were administered. Despite this, the trials were unsuccessful in reducing residual urine to acceptable levels. With addition of therapeutic doses of the drug without the training regimen, voiding trials were also unsuccessful excepting the response of one patient. The drug plus the training regimen was effective in reducing residual urine to acceptable levels in all patients. On discontinuing or decreasing the dosages of the drug, there was gradual but rapid build-up of residual urine despite the active training regimen. Restoration of effective dosage again led to satisfactory voiding function in all patients. The catheter-free group suffered from frequency, nocturia, and bed-wetting owing to excessive residual urine despite the employment of active training regimens. With addition of optimal dosages of Ba-34647, these problems were markedly reduced. They increased with drug discontinuation or dosage decrease and again improved upon restoration of effective doses. Bladder training, including active assistance to the expulsion of urine, is essential to the evaluation of antispasticity drugs for their effect on voiding.

Urinary manometry in patients with spinal cord injury: neurourological considerations in the rehabilitation of acute and chronic neurogenic bladder.

Recordings of pressure within the bladder, urethra, rectum, and external anal sphincter with image intensification and videotaping were carried out in spinal cord injury patients with complete and incomplete lesions, during spinal shock and in the chronic stage. The behavior of the external urethral sphincter and the somatic and visceral motor reflexes of the sacral segments were studied, during and after spinal shock. During spinal shock the majority of patients retained sacral somatomotor activity, in the absence of visceromotor activity, and resistance values at the external urethral sphincter remained high. Vascular oscillations were recorded in the membranous urethra. The highest resistance found in the membranous urethra was at the distal part of the external sphincter.