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Restoration of micturition in patients with acontractile and hypocontractile detrusor by transurethral electrical bladder stimulation.

The aim of transurethral electrical bladder stimulation (TEBS) treatment in patients with diminished detrusor contractility is to attain complete voiding, i.e., micturition without residual urine, which is under volitional control. In contrast to other types of electrical bladder stimulation, the physiological basis for this kind of treatment is sensitizing of the bladder mechanoreceptor afferents. The latency of afferent stimuli in normal conditions indicates that myelinated A-delta-fibers are used for neurotransmission from these mechanoreceptors. Forty-eight patients with hypocontractile or acontractile detrusor underwent intravesical electrical stimulation. All patients had a history pointing to neurogenic pathology. Forty patients had an acontractile and 8 a hypocontractile bladder. Prior to therapy, the mean residual urine volume was 461 ml. After stimulation, 32 of 48 patients were able to void with a mean residual of 57 ml. Detrusor contraction was achieved in 39% and bladder sensation was perceived by 75% of patients who failed these conditions before treatment. Following therapy, 19 of 35 patients were able to empty their bladder without the previously needed catheterization. Side effects were epididymitis in 1 and cystitis in 7 patients.

Adult↗

Client reasons and experiences in treatment that influence termination of psychotherapy.

Thirty-one male and female university counseling center clients completed questionnaires that identified reasons for termination and experiences in psychotherapy. Early terminators responded that they ended therapy because of situational constraints and discomfort with services more often than did late terminators. Late terminators said they stopped treatment because of improvement attributed to therapy more often than did early terminators. Late terminators also reported higher levels of belief that the therapist respected them, therapist warmth, and therapist competency than did early terminators. It was concluded that motivational factors in which volition plays a greater (reasons for termination) and lesser (client experiences) role combine to influence psychotherapy termination.

Adaptation, Psychological↗

Human muscle function and fatigue.

Fatigue is defined as a failure to maintain the required or expected force. The force of a voluntary contraction is graded according to both the tension generated in each muscle fibre and the number of fibres recruited. The same is true of fatigue. Percutaneous electrical stimulation of a muscle via its motor nerve allows the contractile function to be measured independently of volition. Studies have been made of the forces generated isometrically at different stimulation frequencies (frequency: force curve), and of fatiguability (tendency to lose force in a given time at specified stimulation frequencies), in the quadriceps and adductor pollicis muscles. Electrical stimulation recordings of the programmed stimulation myograms distinguish forms of muscle fatigue. Low frequency fatigue which implies impaired excitation-contraction coupling is long-lasting, whereas high frequency fatigue which represents impaired muscle membrane excitation recovers rapidly. Electromyographic (EMG) indicators of fatigue are well recognized but their use is limited because they cannot alone indicate whether alterations in excitation-contraction coupling underlie fatigue. Alterations in the power spectrum of the EMG precede (force) fatigue in sustained maximum voluntary contractions. Fatigue may ultimately be due to a failure of the rate of energy supply to meet demand, but the precise expression of this defect may vary, such that failure of excitation or of activation may predominate over failure of the energy supply.

Energy Metabolism↗

Impaired activation of the supplementary motor area in Parkinson's disease is reversed when akinesia is treated with apomorphine.

Using positron emission tomography (PET) we previously showed that activation of the putamen, supplementary motor area, and cingulate cortex is impaired in patients with Parkinson's disease (PD) when they are off treatment and perform volitional motor tasks. Evidence suggests that these areas are involved in the generation of internally cued movements in normal subjects. We have now studied the effect of the dopamine agonist apomorphine on cerebral activation when used to treat the akinesia of PD. Regional cerebral blood flow was measured using C15O2 PET in PD patients at rest and when performing paced joystick movements with the right hand in one of four freely chosen directions. All patients used apomorphine regularly, and were studied before treatment, while still "off" but receiving a subcutaneous apomorphine infusion, and when switched "on" with apomorphine. Significant increases in regional cerebral blood flow were determined using statistical parametric mapping. Under resting conditions apomorphine had no effect on focal or global cerebral blood flow. Seven patients with PD performed the motor task adequately in the "off" and "on" states. This group of subjects demonstrated impaired activation of the supplementary motor area and contralateral putamen in the "off" state. Activation of the supplementary motor area significantly improved when the akinesia was reversed with apomorphine. We conclude that the concomitant improvement of supplementary motor area activation and motor function in apomorphine-treated patients with PD provides further evidence for the role of this structure in generating motor programs.

Adult↗

Pallidotomy increases activity of motor association cortex in Parkinson's disease: a positron emission tomographic study.

Stereotactic posteroventral pallidotomy can improve motor performance in Parkinson's disease. Interruption of inhibitory pallidal projections to ventrolateral thalamus, components of a cortical-basal ganglia motor loop allows for this clinical benefit. We hypothesized that pallidotomy would lead to increased movement related activity in motor cortical areas receiving projections from ventrolateral thalamus. This was tested in 6 Parkinson's disease patients who underwent stereotactic posteroventral pallidotomy. Each patient was imaged with positron emission tomography (PET) measures of regional cerebral blood flow (rCBF) during performance of a simple prehension task and at rest. Scans were acquired before and 17 weeks after surgery. After pallidotomy, movement-related changes of rCBF increased significantly in both the supplementary motor area (SMA) and premotor cortex but not in primary motor cortex. The results demonstrate the importance of pallidothalamic circuitry for regulating volitional movements and confirm that disruption of inhibitory input to the ventrolateral thalamus can augment movement-related activity in motor association areas.

Adult↗

Aerobic fitness in patients with fibrositis. A controlled study of respiratory gas exchange and 133xenon clearance from exercising muscle.

Aerobic fitness was evaluated in 25 women with fibrositis, by having them exercise to volitional exhaustion on an electronically braked cycle ergometer. Compared with published standards, greater than 80% of the fibrositis patients were not physically fit, as assessed by maximal oxygen uptake. Compared with matched sedentary controls, fibrositis patients accurately perceived their level of exertion in relation to oxygen consumption and attained a similar level of lactic acidosis, as assessed by their respiratory quotient and ventilatory threshold. Exercising muscle blood flow was estimated by 133xenon clearance in a subgroup of 16 fibrositis patients and compared with that in 16 matched sedentary controls; the fibrositis patients exhibited reduced 133xenon clearance. These results indicate a need to include aerobic fitness as a matched variable in future controlled studies of fibrositis and suggest that the "detraining phenomenon" may be of relevance to the etiopathogenesis of the disease.

Adult↗

Impaired growth hormone secretion in fibromyalgia patients: evidence for augmented hypothalamic somatostatin tone.

OBJECTIVE: To determine whether female fibromyalgia (FM) patients exhibit a normal growth hormone (GH) response to an acute exercise stressor, and to assess the importance of somatostatin tone in the generation of this GH response. METHODS: Twenty female FM patients were compared with 10 healthy female controls. All subjects exercised to volitional exhaustion on a treadmill. A standard metabolic cart was used to monitor pulse, blood pressure, electrocardiography, oxygen uptake, carbon dioxide output, anaerobic threshold, and maximal workload. Blood was drawn for GH and cortisol measurements 1 hour before exercise, immediately before exercise, immediately after exercise, and 1 hour after exercise. One month later, testing that was exactly similar was performed, except all subjects were given pyridostigmine bromide (Mestinon; 30 mg orally) 1 hour before exercise. RESULTS: Compared with controls, FM patients failed to exhibit a GH or cortisol response to acute exercise (P = 0.003). After administration of pyridostigmine, 1 hour before exercise, the GH levels of FM patients increased 8-fold (P = 0.001), to a value comparable with that of controls. Pyridostigmine did not increase the cortisol response to exercise in FM patients. Pyridostigmine alone did not stimulate GH secretion in FM patients, nor did it improve exercise-induced GH secretion in controls. FM patients with normal insulin-like growth factor 1 (IGF-1) levels had an impaired GH response to exercise. CONCLUSION: Three new findings are reported: 1) FM patients have a reduced GH response to exercise, 2) pyridostigmine reverses this impaired response, and 3) defective GH secretion in FM can occur in patients with normal IGF-1 levels. Because pyridostigmine is known to reduce somatostatin tone, it is surmised that the defective GH response to exercise in FM patients probably results from increased levels of somatostatin, a hypothalamic hormone that inhibits GH secretion.

Adult↗

The inhibition of automatic saccades in early infancy.

Adult patients with damage centered around the frontal eye fields are severely impaired in the ability to suppress unwanted automatic saccades and in the ability to make volitional eye movements. Over the first few weeks of life most saccades generated by infants appear to be automatic, and are triggered in response to exogenous factors. In the first experiment, the ability of 4-month-old infants to inhibit automatic saccades was studied by exposing them to a series of trials in which a peripheral cue stimulus predicted the location (opposite) in which a colorful, dynamic target stimulus appeared. The results indicate that 4-month-old infants are able to learn to inhibit automatic saccades to a peripheral stimulus, implying maturation of the frontal eye fields by this age. The results of Experiment 2, in which there was no contingent relationship between the cue and target, indicated that the decline in orienting to the cue observed in the first experiment was not due to differential habituation to the less-complex stimulus.

Attention↗

Neuropsychiatric interpretations of postencephalitic movement disorders.

This study reviews the impact of encephalitis lethargica (EL) on concepts of behaviour and movement during the 1920s and 1930s. Clinicopathological correlations were imprecise but supported the role of subcortical structures in complex patterns of motor behaviour. This possibility challenged the widely assumed hegemony of the cerebral cortex. There was a perceived link between involuntary movements and reduced impulse control and also between parkinsonism and a defect in volition. Contemporary observers interpreted postencephalitic phenomena such as oculogyria in psychodynamic as well as in neurophysiological terms. EL also gave some support to the idea that neuroses such as obsessional neurosis and hysteria might have an organic basis. These speculations recently have acquired more credibility. The large amount of literature on EL and its sequelae could perhaps make further contributions to understanding the pathology of voluntary movement and action.

Acute Disease↗

Complex mechanisms of sensory tricks in cervical dystonia.

Muscle activities in 26 patients with predominantly rotational torticollis were quantified using surface electromyography. In the subgroup of 19 patients with an effective sensory trick, different modes and bilateral locations of trick application led to significant (P < 0.002) reduction of electromyographic (EMG) activity. A strong correlation was found between the efficacy of trick manoeuvres and the starting head position. Trick application in a neutral or even contralateral position was most effective while no reduction of muscle activity during trick application at the maximum dystonic head position was found (P < 0.001). We propose a two-phase model: First, normalisation of head posture is obtained by counterpressure or volitional antagonistic muscle activity. In a second step, this position can be stabilised using sensory tricks challenging central adaption of distorted sensorimotor integration.

Electromyography↗

Stiff-person syndrome: an autoimmune disease.

Stiff-person syndrome (SPS) is characterized by progressive, usually symmetric rigidity of the axial muscles with superimposed painful spasms precipitated by tactile stimuli, passive stretch, volitional movement of affected or unaffected muscles, startling noises, and emotional stimuli. Electromyography demonstrates continuous normal motor unit potentials in the affected muscles. Both the rigidity and the spasms are relieved by sleep, general anesthesia, myoneural blockade, peripheral nerve blockade, and partially by diazepam. Evidence for an autoimmune etiology of SPS includes its association with other autoimmune diseases and autoantibodies and the presence of antibodies against glutamic acid decarboxylase (GAD) in the cerebrospinal fluid (CSF) of many affected patients. We describe two patients with this syndrome who had GAD antibodies in both CSF and serum. Partial relief of the symptoms in these patients by corticosteroid therapy provides additional evidence of an autoimmune etiology of SPS and of the role of immunotherapy in its treatment.

Autoantibodies↗

Interlimb coordination in Parkinson's disease.

This study examined the degree to which Parkinson's disease (PD) patients could "spatially link" the upper limbs to facilitate the performance of bimanual simultaneous movements. Six right-handed PD patients, and seven normal age- and sex-matched controls performed three different tasks: (a) an isotonic elbow flexion as rapidly as possible through an angle of 30 degrees; (b) an isometric contraction of the flexor muscles at the elbow joint to 40% and 60% of maximal volitional force (MVF) for a period of 5 s; (c) an isometric contraction for 2.5 s with one limb, then simultaneously performing an isotonic flexion with the contralateral limb while maintaining the isometric contraction for 2.5 s more. As expected, PD patients were significantly slower in performing the isotonic movement and produced lower peak velocities than the controls. More importantly, the two groups were differentially affected during the bimanual condition. In normals, movement time decreased and peak velocity increased in the bimanual condition. In contrast, PD patients showed increased movement times and sometimes decreased peak velocities in the bimanual condition. The results suggest that normal subjects utilize bilateral outflow to symmetrical muscle groups to synchronize the two limbs in the bimanual task, whereas PD patients dissociate the two limbs.

Aged↗

Electrophysiologic findings and muscle strength grading in brachioplexopathies.

The electrophysiological evaluations and the British Medical Research Council (MRC) scale (0-5) findings of target muscles in brachioplexopathies before surgery and 1 year postsurgery were conducted. Each component of the brachial plexus was analyzed in 15 patients with injuries, among them, to 5 roots, 19 trunks, 7 cords, and 13 terminal nerves. In each of these cases, neurolysis and/or nerve transfer and/or neurotization were performed, within 3 weeks to 6 months after the injury was incurred, to ameliorate the resulting severe disabilities. The degrees of impairment were graded using a modified version of Dumitru's and Wilbourn's scale (mild: normal to slight decrease of SNAP amplitude and CMAP amplitude, and occasional denervation; moderate: profound decrease of SNAP amplitude and CMAP amplitude, constant denervation, and normal to slight decrease in motor unit recruitment; severe: absent SNAP amplitude, absent CMAP amplitude, marked denervation, and profound decrease or no volitional motor unit recruitment. mild = 1; moderate = 2; severe = 3). The motor power of the target muscles was graded through MRC scores. The presurgical versus postsurgical differences in the severity of the injury to each brachial plexus component, and differences in the grading of target muscle power, were calculated through the Wilcoxon signed-rank test. The presurgical degrees of the severity of injury, as measured by the electromyography (EMG) were 3.00 +/- 0.00 (mean +/- SD) in root, 2.84 +/- 0.50 in trunk, 3.00 +/- 0.00 in cord, and 2.85 +/- 0.38 in terminal nerves. The postsurgical results were 2.60 +/- 0.55 in root, 2.53 +/- 0.70 in trunk, 2.43 +/- 0.53 in cord, and 1.77 +/- 0.73 in terminal nerves. There was significant improvement at the trunk, cord, and terminal nerve levels after repair, but not at the root levels. Moreover, although the MRC grading showed significant motor recovery in the infraspinatus, deltoid, biceps, and triceps muscles, there was little apparent improvement in the pectoralis major, EDC, APB, and ADM muscles. Nerve repair was notably successful in all plexuses except at the root level. However, our cases demonstrated only poor motor power gains in the forearm and the hand muscles. Consequently, future surgical techniques for brachioplexopathy repairs need further improvement.

Adolescent↗

Pathophysiology of spastic paresis. I: Paresis and soft tissue changes.

Spastic paresis follows chronic disruption of the central execution of volitional command. Motor function in patients with spastic paresis is subjected over time to three fundamental insults, of which the last two are avoidable: (1) the neural insult itself, which causes paresis, i.e., reduced voluntary motor unit recruitment; (2) the relative immobilization of the paretic body part, commonly imposed by the current care environment, which causes adaptive shortening of the muscles left in a shortened position and joint contracture; and (3) the chronic disuse of the paretic body part, which is typically self-imposed in most patients. Chronic disuse causes plastic rearrangements in the higher centers that further reduce the ability to voluntarily recruit motor units, i.e., that aggravate baseline paresis. Part I of this review focuses on the pathophysiology of the first two factors causing motor impairment in spastic paresis: the vicious cycle of paresis-disuse-paresis and the contracture in soft tissues.

Contracture↗

Accuracy of predicting maximal quadriceps force from submaximal effort contractions after anterior cruciate ligament injury.

Weakness and failure of voluntary activation of the quadriceps femoris muscles often occur after anterior cruciate ligament (ACL) rupture. Side-to-side strength comparisons are used as a measure of progress, and are inaccurate if the quadriceps has activation failure. Burst superimposition testing is commonly used to assess quadriceps strength and activation during a maximal volitional isometric contraction (MVIC), using the central activation ratio (CAR) calculation. A recently developed mathematical model predicts the MVIC from submaximal efforts. The purpose of this study was to compare the CAR calculation to the mathematical model. We hypothesized that the model would be a more accurate predictor of strength than the CAR calculation when voluntary activation failure is present. Data from the involved and uninvolved quadriceps muscles of 100 consecutive subjects with complete, isolated ACL rupture were retrospectively evaluated. Subjects who required multiple trials to produce an MVIC with full activation (true MVIC) were used to compare the CAR calculation, the mathematical model, and this true MVIC. Subjects unable to produce a true MVIC with multiple trials were used to compare the mathematical model to the CAR calculation. Results demonstrate that both methods reliably and accurately estimate the quadriceps weakness associated with ACL rupture. We recommend use of the CAR calculation to provide estimations of true quadriceps strength to facilitate clinical decisions about progress in rehabilitation after ACL rupture.

Adolescent↗

Acoustic myography: a noninvasive monitor of motor unit fatigue.

Acoustic myography is the recording of sounds produced by contracting muscle. These sounds become louder with increasing force of contraction. We have compared muscle sounds with surface EMG to monitor the dissociation of electrical from mechanical events (presumably, the loss of excitation-contraction coupling) which occur with motor unit fatigue. Acoustic signals were amplified using a standard phonocardiograph, recorded on FM magnetic tape, and digitally analyzed. Muscles were examined at rest, with intermittent contractions, and with sustained contractions. We found that with fatigue, the acoustic amplitude decayed, but the surface EMG amplitude did not. With decreased effort, however, the acoustic and the surface EMG amplitudes declined simultaneously. By simultaneously recording acoustic signals and needle EMG, individual motor units were resolved acoustically in two muscles with decreased numbers of motor units and increased motor unit size. Fasciculations also produced acoustic signals, although no acoustic signal has yet been found that correlates with fibrillations. Analysis of acoustic signals from muscle provides a noninvasive method for monitoring motor unit fatigue in vivo. It may also be useful in distinguishing muscle fatigue from decreased volition.

Acoustics↗

Synchronous positive and negative myoclonus due to pontine hemorrhage.

We report a case of synchronous positive and negative myoclonus following pontine hemorrhage. Constant synchronous jerking of the eyes, tongue, face, mandible, larynx, pharynx, and diaphragms persisted during sleep. Jerking of limb muscles occurred during volitional activities, but not at rest. Inability to sustain glottic adduction during phonation contributed to severe dysarthria. Electromyography (EMG) revealed positive myoclonus of the branchial musculature with synchronous negative myoclonus in a generalized distribution. Treatment with trazodone reduced the ocular myoclonus but worsened the dysphagia. We suggest that a single neural rhythm generator may produce both positive and negative myoclonus.

Adult↗

Muscle cramp as the result of impaired GABA function--an electrophysiological and pharmacological observation.

We investigated the mechanism of cramps in 2 patients: a 48-year-old man with bulbospinal neuronopathy, and a 46-year-old man with amyotrophic lateral sclerosis. Cramps were quite easily induced by volitional exertion and high-frequency stimulation of the peripheral nerves. When an ulnar nerve was blocked with lidocaine at the elbow, no cramp was induced despite the application of high-frequency stimulation at the wrist. Diazepam (GABAA agonist) was effective in the first patient and baclofen (GABAB agonist) in the second, with no cramps induced in spite of increasing stimulation intensity. Impairment of interneurons mediated by GABA as the neurotransmitter is thought to be involved in the mechanism of the cramps.

Amyotrophic Lateral Sclerosis↗