A calcium blocking and anticholinergic agent (terodiline) in the treatment of detrusor hyperreflexia: a placebo-controlled, cross-over trial.

In 25 neurological patients with detrusor hyperreflexia terodiline reduced the number of total micturitions during daytime. Bladder capacity was increased and amplitude of the bladder contractions was reduced. An increase in residual urine was also observed. Mild anticholinergic side-effects were measured on pupillary motility and on heart rate variation. It is concluded that terodiline is a useful alternative in treatment of patients with detrusor hyperreflexia.

[Effect 4-aminopyridine on the recovery of segmental reflexes after sectioning of the sciatic nerve in the rat]. / Vliianie 4-aminopiridina na vosstanovlenie segmentarnykh refleksov posle pererezki sedalishchnogo nerva u krys.

L5 ventral root reflex discharges evoked by dorsal root stimulation were studied 3-4 weeks after transection of sciatic nerve in rats; only polysynaptic transmission was found on the side of operation. Injection of 4-aminopyridine (500-600 mg/kg, intraperitoneally) resulted in facilitation of reflex discharges on the intact side and in reappearance of intensive monosynaptic component in such discharges on the affected side. It is concluded that 4-aminopyridine recovers monosynaptic transmission between primary afferents and chromatolysed motoneurons because of increased transmitter liberation.

[Clinical studies of autonomic hyperreflexia].

Autonomic hyperreflexia in 25 patients with spinal cord injury has been clinically analyzed. Nineteen of the patients (76%) suffered from neurogenic lesions above Th-5 and the rest (24%) below Th-6. The most frequent subjective symptom was sweating (22 patients), followed by headache, nausea and so forth. These symptoms were encountered mostly in patients with poor voiding efficiency and developed less than one year after the spinal cord injury. Both systolic and diastolic blood pressure elevated with the distension of the bladder. At the maximum bladder capacity both systolic and diastolic pressure were 39% higher than that observed in the empty bladder. Regitin, 10 mg, given intravenously suppressed this elevation by two-thirds compared to the control. The treatment modality consisted of clean intermittent catheterization and external sphincterotomy, to prevent the over-stretching of the detrusor muscle, together with administration of alpha-adrenergic blockers and ganglionic blocking agent, which interrupt the efferent impulse. Twenty two of the patients (88%) were successfully controlled.

Effect of naloxone on the defective autonomic control of heart rate in uraemic patients.

The role of endogenous opioids on the reflex cardiovascular control of chronic uraemic patients was investigated. The opiate antagonist naloxone administered intravenously caused a significant increase in the abnormal Valsalva manoeuvre ratio in nine chronic uraemic patients, but it had no effect in six diabetic patients with normal renal function, whose response to the Valsalva manoeuvre was similar to that of chronic uraemic patients. Naloxone had no effect in eight normal subjects. The increase in the Valsalva ratio observed in uraemic patients was due to restoration of the parasympathetically mediated reflex bradycardia of the release phase of the manoeuvre. Naloxone did not modify supine and standing blood pressure and heart rate in any group. Endogenous opioids may be involved in the defective autonomic control of heart rate in uraemic patients.

[Pharmacological study of the temporary cerebral ischemic rats produced by bilateral vertebral and carotid artery occlusion. Effects of DN-1417].

We investigated the ameliorating effects of DN-1417 (a TRH analog) on the changes of behavior, EEG, neurochemical parameters and regional cerebral blood flow (rCBF) in rats with global cerebral ischemia. Global cerebral ischemia was produced by 10-min occlusion of both common carotid arteries 24 hr after the permanent electrocauterization of bilateral vertebral arteries. DN-1417 was administered intraperitoneally as soon as possible, following recirculation of carotid blood flow. DN-1417 shortened significantly the recovery times of righting reflex (RR) and spontaneous movement (SM) at 2.5 mg/kg and higher doses, and it recovered effectively the EEG activity at 10 mg/kg during recirculation after 10-min cerebral ischemia. In addition, DN-1417 (10 mg/kg) recovered the various changes such as decrease of 5-hydroxytryptamine (5-HT) levels, increase of cyclic AMP (cAMP) levels, inhibition of [3H]-choline uptake, depression of choline acetyltransferase (CAT) and acetylcholine esterase (AChE) activities, and shortened the durations of hyperperfusion and hypoperfusion of rCBF. As a result, it is identified that DN-1417 ameliorates the disturbance of consciousness supposedly caused by behavioral and EEG abnormalities during recirculation following the temporary cerebral ischemia, and the effect of DN-1417 seems to be mediated by normalizing of alterations in the brain monoaminergic and cholinergic systems, as well as rCBF, and the effectiveness for disturbance of consciousness in clinical situations would be expected.

Intradiscal collagenase for treatment of lumbar disc herniations. A comparison of clinical results and computed tomography follow-up.

In a series of 34 patients with herniated lumbar discs, treated by intradiscal injection of highly purified collagenase, the post-treatment course has been followed-up clinically and by repeated computed tomographies (CT). Good or excellent results have been achieved in 17 patients. An only slight improvement of pain was noted in 2 patients. Fifteen patients had to be operated on due to not improved or worsened clinical symptoms. The most striking result of our CT follow-up was a tendency of the disc herniation to increase initially after collagenase injection. About two thirds of the patients had such an increase at the one week after injection control. After 6 weeks this rate had decreased to only about one quarter, but in the meantime 13 patients had to be operated. Only after 6 months most hernias of the up till then not operated patients were smaller and none were larger than before treatment. There was also a transient density decrease of the treated disc, most pronounced one week after collagenase injection. At controls 6 months later density had reached again pre-treatment levels. It is likely that the volume increase tendency of the disc material after collagenase injection is responsible for a worsening of the clinical symptoms, which not seldomly occurs during the initial post-treatment period, and in some patients makes an operation necessary.

Restoration of normal reflex responses to orthostatic stress during felodipine therapy in congestive heart failure.

The mechanisms underlying the abnormal responses to orthostatic stress in congestive heart failure are ill defined and little is known about the effects of specific therapy. In the present study intravascular pressures and plasma noradrenaline levels were measured in nine patients with heart failure subjected to 45 degrees and 90 degrees upright tilt. Studies were repeated during 4 weeks of vasodilator therapy with felodipine and again after felodipine withdrawal. Before the introduction of vasodilator therapy, tilt did not activate orthostatic reflexes despite significant reductions in left ventricular filling pressure and cardiac output. Thus, plasma noradrenaline, heart rate and systemic vascular resistance were unaffected and blood pressure fell. Felodipine resulted in a rapid and sustained improvement in left ventricular function but restoration of orthostatic reflexes was delayed and could be detected only after 48 h therapy. At this time, and during the subsequent 4 weeks, tilt-induced reductions in ventricular filling and cardiac output produced a normal rise in plasma noradrenaline and heart rate. A postural drop in blood pressure, however, was not averted because the direct action of felodipine on vascular smooth muscle prevented adrenergically-mediated increments in systemic vascular resistance. Felodipine withdrawal led to a prompt deterioration in left ventricular function. Orthostatic reflexes, however, were still intact 48 h later when tilt elicited a completely normal pattern of responses. These observations confirm that the abnormal responses to orthostatic stress in congestive heart failure are due principally to impairment of autonomic control mechanisms and are not related to the absence of venous pooling. Importantly the autonomic dysfunction is reversible with felodipine therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Autonomic dysreflexia (hyperreflexia).

This author has presented his personal experience and observations concerning acute and chronic dysreflexia. The various causes of dysreflexia are discussed. The importance of bladder balance is stressed as the number one cause with the anorectal site being second. The methods of treatment that the author uses for both acute and chronic dysreflexia are described.

[Clinical impact of the Bezold-Jarisch reflex in coronary arteriography]. / Repercusiones clínicas del reflejo de Bezold-Jarisch en la arteriografía coronaria.

To evaluate the role that coronary arteriography has in the induction of the Bezold-Jarisch reflex we study 9 patients (group I) to whom 1 mg. of atropine was administered 45 min. before the coronary arteriography and 9 patients (group II) without pre-medication. The heart rate was measured before, during and after each intracoronary injection. In group I there was no change in heart rate in 6 patients, in 3 cases the heart rate dropped to 15 beats/min. In group II the heart rate decreased in 8 cases. We conclude that the injection of radiologic contrast material in the coronary arteries triggers the Bezold-Jarisch reflex and that this reflex is prevented by the administration of atropine.

Treatment of acute autonomic dysreflexia.

Chlorpromazine has proved useful in the control of sustained dysreflexia in patients with spinal cord injury. Sustained autonomic dysreflexia can be life threatening and may occur after dysfunctional urethrovesical activity or after urological operations, such as external sphincterotomy. Given by injection chlorpromazine reduced blood pressure safely and effectively.

Dysfunction of the detrusor and urethra in multiple sclerosis: the role of drug therapy.

Urinary tract disorders secondary to multiple sclerosis are common. In this series of 24 patients with multiple sclerosis, 5 had normal function of the detrusor, 3 had detrusor hypotonicity and 16 had detrusor hyperreflexia. The proximal urethra was evaluated using radiologic and electromyographic techniques. These studies showed that 5 patients had a normal urethra, 15 had some degree of somatic dyssynergia and 3 had sympathetic dyssynergia. Detrusor hyperreflexia with somatic dyssynergia was found in 11 patients and was the most common pattern. The therapeutic response to standard pharmacologic preparations was also evaluated. The regimen was based on the clinical and urodynamic findings for each patient. Dicyclomine hydrochloride was the drug of choice for detrusor hyperreflexia, bethanechol chloride for hypotonicity, dantrolene sodium for somatic dyssynergia and phenoxybenzamine hydrochloride for sympathetic dyssynergia. The authors found that most of their patients were amenable to drug therapy, the exception being those with advanced neurologic lesions.

Management of vesical dysfunction in multiple sclerosis.

Using urodynamic testing, vesical dysfunction in patients with multiple sclerosis can be classified and basic therapeutic principles outlined. Satisfactory voiding patterns can be achieved in most patients with multiple sclerosis without surgical procedures. Flexibility and willingness to change programs as the disease process changes make possible reasonably satisfactory results.