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Two patients with chronic hypertonus (in a decerebrate state) as a result of hypoxia are described. Long-term cerebellar stimulation markedly modified their extraordinarily severe extensor-flexor rigidity phenomena that had resulted in chronic opisthotonus.
Induction of hypothermia is used routinely in neurosurgical and cardiovascular operations to protect the brain from ischemic insult. However, despite a plethora of experimental evidence supporting the use of hypothermia to protect the brain from ischemia, clinical experience using deliberate hypothermia in humans has not shown a convincing benefit. The authors tested the hypothesis that hypothermia and rewarming alter tone in human cerebral vessels and may interfere with cerebral perfusion in the setting of deliberate hypothermia. They examined human cerebral arteries during hypothermia (32 degrees C and 17 degrees C) and during rewarming to delineate the direct effects of cooling and rewarming on cerebrovascular tone. Artery segments obtained from autopsy material and from specimens excised at elective temporal lobectomies were tested in tissue baths using isometric tension measurements. Temperature-induced changes in vascular tone were measured and quantified with respect to contractile responses to serotonin (5-HT; 10(-6) M). Cooling induced mild relaxation in cerebral vessels (-38 +/- 12% 5-HT response in 50 vessels from autopsy specimens, -69 +/- 10% 5-HT response in 51 vessels from lobectomy specimens). On rewarming, vessels contracted significantly beyond their baseline tone (108 +/- 18% 5-HT response in 50 vessels from autopsy specimens, 42 +/- 12% 5-HT response in 51 vessels from lobectomy specimens). Rewarming-induced hypercontractility was inhibited by the tyrosine kinase inhibitor genistein (-5 +/- 7% vs. 70 +/- 23% 5-HT response, genistein vs. control, 14 segments, p < 0.05) and enhanced by the tyrosine phosphatase inhibitor sodium orthovanadate (339 +/- 54% vs. 104 +/- 20% 5-HT response, sodium orthovanadate vs. control, five segments, p < 0.05), indicating a possible role for tyrosine kinase activation in the rewarming-induced contraction.
Snook's spasticity reduction splint was evaluated objectively with five severely and profoundly handicapped subjects. The force of spastic wrist flexors in pounds of pull was measured on a spring-weighted scale. Findings demonstrated that the device designed for this study was useful in measuring hypertonus; splint wearing resulted in a reduction of the passive component of muscle tone and that this reduction was related to the length of time the subjects wore splints; the effects of splint wearing were not necessarily permanent. Components that contribute to the condition of hypertonicity are discussed, as well as the implications of the study findings for occupational therapists.
Positioning and seating are important for premature and young infants with tonal problems. Positioning with pillows and sandbags, the use of special handling techniques (Bobath's neural developmental treatment), as well as other specialized approaches, have not proved satisfactory in reducing tone or spasticity in these infants. We developed an adaptive seat designed to reduce extensor tone through proper positioning. This seat has also been helpful in diminishing agitation. Without these benefits, infants are often immobilized in extension and cannot actively explore their environments. Diminution in agitation has also been important in increasing interaction with nurses.
INTRODUCTION: Ischemic anoxic cerebral crises are linked to cardio-inhibition in response to vagal hypersensitivity which causes cerebral ischemic. OBJECTIVE: In this paper we proposed to describe the clinical and electrophysiological features seen during the ocular compression test. PATIENTS AND METHODS: We studied 200 children with clinical findings suggesting ischemic anoxic cerebral crises with positive results on ocular compression testing. RESULTS: The ocular compression test provoked signs and symptoms, on average, in between 48.5% and 62.5% of the patients; generalized hypotonia and loss of consciousness were the most frequent signs. We found that the presence of clinical changes depended on the duration of the pause in heartbeat. There was also an association between the duration of the pause in heartbeat and the electroencephalographic findings. CONCLUSIONS: Identification of a state of vagal hypersensitivity is of considerable value in the positive differential diagnosis of cerebral crises in children, and of definite prognostic value.
After depletion of intracellular calcium stores sensitive to noradrenaline, a spontaneous increase in the resting tone (IRT) when incubated in Ca(2+)-containing solution was observed in isolated rat aorta, but not in tail artery. This IRT does not depend on agonist activation of alpha(1)-adrenoceptors but it is inhibited by prazosin. A close relationship was found between the inhibitory potencies of prazosin (pIC(50) = 9.833), BMY 7378 (pIC(50) = 8.924), and 5-methylurapidil (pIC(50) = 7.883) against IRT and their affinities for cloned alpha(1D)-adrenoceptors. Chloroethylclonidine (100 micromol. l(-1)) did not inhibit the IRT. After depletion of internal calcium stores by noradrenaline in absence of the agonist, loading in Ca(2+)-containing solution also brings about an increase in the inositol phosphate (IP) levels in rat aorta (not seen in tail artery) that is inhibited by prazosin (1 micromol. l(-1)), BMY 7378 (10 micromol. l(-1)), and 5-methylurapidil (10 micromol. l(-1)), thus confirming the results obtained in contractile studies. Chloroethylclonidine (100 micromol. l(-1)) did not inhibit this IP accumulation. The fact that the IRT and the IP accumulation related to it can be selectively inhibited by different alpha(1)-adrenoceptor antagonists suggests the existence of a population of alpha(1D)-adrenoceptors that show constitutive activity in rat aorta, not in tail artery.
PURPOSE: Management of idiopathic detrusor instability is difficult in most patients mainly due to the lack of a complete understanding of the pathophysiology. Oxybutynin and transcutaneous electrical nerve stimulation have been used but to our knowledge no direct comparisons have been made. MATERIALS AND METHODS: Patients with frequency, urgency, urge incontinence and proved detrusor instability were studied with urodynamics, quality of life instruments, and frequency and volume charts. Patients were randomized to transcutaneous electrical nerve stimulation or oxybutynin. After 6 weeks of treatment, they were reassessed and after a washout of 2 weeks, they were started on the second arm of treatment and reassessed 6 weeks later. RESULTS: A total of 13 male and 30 female patients were studied. Functional capacity had increased and number of voids daily had decreased significantly compared with before treatment in both arms (p <0.005). There were significant improvements in symptom specific quality of life measures but no changes were found on the global Short Form 36 (SF-36) quality of life questionnaire. The volume to first desire to void and first unstable contraction had increased significantly with oxybutynin but not with transcutaneous electrical nerve stimulation. Of 23 patients 7 were stabilized with treatment, including 2 with oxybutynin only, 2 with either nerve stimulation or oxybutynin and the remaining 3 with only nerve stimulation. Total bladder capacity did not change significantly with either treatment but patients noticed side effects more commonly with oxybutynin. CONCLUSIONS: Both treatments clearly improved subjective parameters. However, only oxybutynin showed significant improvements in objective urodynamic parameters. Transcutaneous electrical nerve stimulation can be used in patients who cannot take oxybutynin. Further studies are needed to show the long-term efficacy and cost analyses of nerve stimulation.
In this work the authors reported the case of a 29-year-old woman, who had been dialysed since 1997 in the course of chronic pyelonephritis caused by vesicoureteral reflux. Due to the detrusor vesica urinariay's hypofunction (confirmed by repeated urodynamic studies) the patient was prescribed Baclofen with a dosage of 2 x 10 mg per 24 hours. In the course of Baclofen's therapy, toxic effects of the drug like weakness, nausea, vomiting and fears appeared during the second day of treatment. They had been increasing since the patient's admission to the Dialysis Centre where she had immediately undergone the planned haemodialysis. After the initial increase of the poisoning symptoms including the loss of consciousness, patient's state of health improved after approximately two hours since the haemodialysis had been performed. After five more days in hospital, the patient was discharged in general good condition (two more planned haemodialyses were performed at the time of treatment).
To investigate excitability of spinal neural function during stretching excises in patients with cerebrovascular disease (CVD), H-reflex was analyzed before, during and after 1 min. continued stretching of the affected arm. 10 hemiparesis patients with hypertonus and hyperreflex, mean age of 53.2 years were tested. H-reflex was recorded from the abductor pollicis brevis on the affected side after stimulation of median nerve in supine position. The persistence, amplitude and amplitude ratio of H/M during stretching were lower than those before and after in the patients with moderately increased muscle tonus. In patients with slightly and markedly increased, H-reflex was same before, during and after continued stretching. It is suggested that excitability of spinal neural function during 1 min. continued stretching was inhibited in the patients with moderately increased muscle tonus caused by CVD.
To investigate the effect of continued stretching of affected arms in patients with cerebrovascular disease (CVD), F-wave was tested from the abductor pollicis brevis (APB) during relaxation (trial 1) and 3 different continued stretches: stretched position with shoulder abduction (trial 2), stretched position with shoulder abduction and elbow extension (trial 3), and stretched position with shoulder abduction, elbow extension and wrist extension (trial 4) of the affected arm for 1 min. in 20 hemiparesis patients with moderate hypertonus (modified Ashworth scale of 2 or 3) caused by CVD (mean age of 49.5 years). Persistence and amplitude ratio of F/M in trial 2 were the same as those in trial 1. Persistence and amplitude ratio of F/M in trials 3 and 4 were significantly lower than those in trial 1. It was suggested that excitability of spinal neural function of the distal part, the APB, of the affected arm was reduced during continued stretching of the proximal part, shoulder and elbow joints, or all of the shoulder, elbow and wrist joints in hemiparesis patients with moderate hypertonus caused by CVD.
It is a common clinical observation that stretch reflex excitability increases progressively after spinal transsection in man, and causes many severe complications. The purpose of the present study was to investigate the role and mechanism of substance P (SP) on the spinal reflex following spinal cord transsection. We first observed the changes of spontaneous electromyography (EMG) recorded in the paralyzed limbs of spinally transsected rats, and found that the EMG amplitude increased progressively within 40 days. The results were as follows: 1) Spontaneous EMG increased significantly following intrathecal injection of 1 microgram capsaicin, and the sensitivity of EMG to capsaicin increased progressively with time. But this effect could be partly blocked by pretreatment with SP antiserum. 2) Spontaneous EMG increased significantly following intrathecal injection of SP. Yet the time course was relatively short and the amplitude of EMG was lower. These results indicate that SP in the spinal dorsal horn participates in the regulation of myotension, and it is suggested that to decrease SP content in the spinal dorsal horn or block the afferent fibers of dorsal roots might be an effective therapy to reduce the hypermyotension caused by spinal cord injury, multiple sclerosis or other reasons.
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