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PubMed2005

Botulinum toxin: mechanisms of action.

This review describes therapeutically relevant mechanisms of action of botulinum toxin (BT). BT's molecular mode of action includes extracellular binding to glycoproteine structures on cholinergic nerve terminals and intracellular blockade of the acetylcholine secretion. BT affects the spinal stretch reflex by blockade of intrafusal muscle fibres with consecutive reduction of Ia/II afferent signals and muscle tone without affecting muscle strength (reflex inhibition). This mechanism allows for antidystonic effects not only caused by target muscle paresis. BT also blocks efferent autonomic fibres to smooth muscles and to exocrine glands. Direct central nervous system effects are not observed, since BT does not cross the blood-brain-barrier and since it is inactivated during its retrograde axonal transport. Indirect central nervous system effects include reflex inhibition, normalisation of reciprocal inhibition, intracortical inhibition and somatosensory evoked potentials. Reduction of formalin-induced pain suggests direct analgesic BT effects possibly mediated through blockade of substance P, glutamate and calcitonin gene related peptide.

Anti-Dyskinesia Agents↗

PubMed2000

Electric activity spreads in the colonic longitudinal but not the circular musculature. Role in colonic motility.

The colon has a circular and longitudinal muscle layers and possesses an electric activity. The current study investigated the spread of this electric activity in the colonic musculature. The tests were performed in 16 patients (mean age 40.6 +/- 10.8 SD years, 10 men, 6 women) during operative correction of their incisional hernias in the anterior abdominal wall. Three electrodes were applied to the longitudinal muscle of the descending colon, and 3 to the circular muscle. The colonic pressure was monitored by a 10-F tube inserted per anus and connected to a pressure transducer. Electric waves in the form of pacesetter potentials (PPs) and action potentials (APs) were recorded from the longitudinal but not the circular muscle coat. The PPs and APs had the same frequency, amplitude and conduction velocity from the 3 electrodes of the same patient. The APs were associated with a rise of the intracolonic pressure. The results were reproducible in the individual subject. Being of the visceral type, the colonic smooth muscle fibers are controlled by non-nervous stimuli. Colonic motility is suggested to be effected by means of 2 mechanisms: the longitudinal muscle fibers activity through the action of the electric waves and the circular muscle fibers through the stretch reflex.

Action Potentials↗

PubMed1978

Cerebellar stimulation in man. Quantitative changes in spasticity.

The effects of chronic anterior lobe cerebellar stimulation on patients with cerebral palsy have been investigated using a new method of quanitfying muscle rigidity and stretch reflexes. The ankle is oscillated sinusoidally, compliance is measured at several frequencies, and electromyographic activity of the extensor and flexor muscles is recorded. In some patients stimulation can reduce rigidity and coactivation of muscles immediately or slowly over days or months. In others no change is found.

Adolescent↗

PubMed1999

Contribution of motor unit activity enhanced by acute fatigue to physiological tremor of finger.

The contribution of motor unit activity to a physiological tremor (hereafter called as tremor) in a middle finger is studied by both a power spectrum and a correlation analysis in which the correlation coefficient and the coherence spectrum are obtained when five kinds of loads, 0, 50, 100, 150, and 200 g, are added to the middle finger for two minutes in a loading experiment on twelve male subjects. A weight of 200 g is applied to the subjects for ten minutes in a fatigue experiment. Throughout both experiments, the middle finger remains stretched from the load of the weight. The tremor is measured by an accelerometer (MT-3T, Nihon Kohden, Japan) attached to the middle finger, and the surface electromyogram (EMG) is measured by bipolar electrodes placed on m. extensor digitorum communis. A power spectrum analysis is carried out on the tremor and EMG, and a correlation analysis is performed on the relationship between the tremor and the demodulated EMG. It is found in the loading experiment that when the weight on the finger increases, the amplitude of the tremor oscillation increases since the activity of the motor units of the muscle is enhanced by the phenomenon of recruitment. Two frequency components of the tremor spectra at 10 Hz and 25 Hz under a no load condition reflect the components of the activity of the motor units of the muscle because the tremor shows a significant correlation in the frequency zone of 10 Hz and 25 Hz with the demodulated EMG. The lower frequency component of the tremor spectrum at 10 Hz results in synchronized activity of the motor units, while the higher frequency at 25 Hz occurs from the stretch reflex loop via the motoneurons of the spinal cord. The shift of the higher frequency component to the lower frequency domain due to the load of the weight originates from the prolongation of the response time of the finger mechanical system because the lag time at the peak of the correlation coefficient increases with the load of the weight. It is found in the fatigue experiment that the amplitude of the tremor oscillation increases with the progress of fatigue. The increase is caused by the recruitment of the motor unit activity of the muscle holding the finger as well as by the synchronization of the firings of the motoneurons. The progress of the synchronization is verified by the fact that the mean power frequency (MPF) of the EMG spectrum decreases and the correlation between the tremor and the demodulated EMG increases with the progress of fatigue. The mechanisms of the increase of the amplitude of the tremor oscillation under the load of the weight to the finger and under the state of fatigue of the finger are elucidated by the analysis of the tremor and EMG.

Adult↗

PubMed1975

[Methods for recording and quantitative measurement of rigidity and spasticity (author's transl)].

First pathophysiological aspects of rigidity and spasticity are described with special regard to the possibilities of errors during the measurement of muscle tone in man. The following methods are explained and discussed: Psychometric techniques, physical analysis of movements (kinesiology, photobadismography, kinetometry), pendulousness tests, investigations of reflexes (T-reflex, H-reflex, H/M-ratio), electromyographic methods (after-activity, silent period, unloading-reflex, stretch-reflex, release-phaenomen), and torque measurements. In the main we discussed these techniques with the view-point of diagnosis and drug effects. Furthermore we expressed our opinion on the relevance of the different methods. Last the most important sources of errors are tabulated.

Electromyography↗

PubMed1989

[Differential diagnosis of Friedreich ataxia].

The clinical records of 72 patients with spinocerebellar ataxias which had manifested before the age of 20, were examined in a retrospective study. Depending on whether the muscle stretch reflexes in the legs were positive or negative, two groups were distinguished, that of early onset cerebellar ataxia with retained tendon reflexes (EOCA) (13 P.) and that of Friedreich's ataxia (FA) (59 P.). The clinical course was much worse in the FA patients compared with EOCA. Cardiomyopathy and diabetes mellitus were not a feature of EOCA. Scoliosis and a disturbed position sense in the toes were more frequent in FA cases. The striking differences in clinical signs and course of the diseases justify the differentiation of EOCA from FA, as suggested by Harding in 1981.

Adolescent↗

PubMed1987

Spasticity.

Spasticity has been defined as velocity-dependent hyperactivity of stretch reflexes; it is therefore only one aspect of the complex syndrome produced by a lesion of the upper motoneuron. Although spasticity may be partially responsible for joint contractures, it does not produce most of the functional disability experienced by patients with upper motoneuron lesions. Paresis, fatigability, lack of dexterity, etc., account for most of these patients' complaints. The pathophysiology of spasticity is poorly understood but appears to be related to an increased excitatory state at the segmental spinal level; there is no evidence for increased sensitivity of muscle spindles in spastic patients. Several mechanisms for this increased excitability within the spinal cord have been proposed. There are different types as well as degrees of spasticity. Clinical neurophysiologic recordings of reflex activity in patients with spasticity provide the means to differentiate among the various types of spasticity, to select the therapy most likely to be effective in a particular patient, and to see the results of its employment objectively. The latter will prove whether a specific therapy is useful or not. Ablative treatment at the level of the peripheral nerve or dorsal root may be useful, particularly when spasticity is severe. Drugs such as baclofen or diazepam relieve flexor spasms but are not particularly effective against spasticity itself. Dantrolene acts to weaken muscles, but that is not often helpful. Rarely do any of these therapies increase function; there are no effective cures for paresis or related negative manifestations of chronic spasticity.

Combined Modality Therapy↗

PubMed1977

Adie's syndrome: some new observations.

Adie's syndrome is a disease of unknown etiology. We known where the damage is, and which nerves are involved. We even know something of how the nerves react after the damage is done, but we don't known what causes the primary injury. The first step in working a jigsaw puzzle is to getall of the pieces right side up and take a good look at them. Some of the jigsaw pieces handled in this paper are listed below. Some of them are new observations; many of them are old concepts, partly modified and partly made secure by new facts. 1. Not all "tonic pupils" are due to "Adie's syndrome"; some are due to local injury and some to a generalized peripheral neuropathy (Table II). 2. All patients should have serologic tests for shyphilis. In this series one in six had positive serology. 3. The incidence of Adie's syndrome in Iowa in the early 1970's was approximately 4.7 per 100,000 population per year. 4. The prevalence of Adie's syndrome, therefore, was approximately 2 per 1000. 5. The mean age of onset of Adie's syndrome was about 32.2 years (Figure 1A). 6. The sex ratio was 2.6 females to each male. 7. Right eyes and left eyes were involved at approximately the same rate (Figure 2). 8. The incidence of second eye involvement in unilateral cases was about 4% per year during the first decade of the disease (Figure 18). 9. If this rate of second eye involvement (4% per year) persists during subsequent decades, then most Adie's pupils will eventually become bilateral. 10. The incidence of Adie's syndrome in a largely caucasian patient group is independent of iris color (Figure 4). 11. Only 10% of patients with Adie's syndrome had completely normal muscle stretch reflexes. 12. The muscle stretch reflexes in the arms were just as frequently imparied as those in th elegs, but the degree of impariment tended to be more severe in the ankles and triceps. 13. When there was any light reaction remaining in an Adie's pupil, a segmental paralysis of the sphincter muscle could be seen. 14. The near reaction of the pupil was often segmental and frequently involved segments which did not respond to light. 15. The segmental paralysis to light was randomly distributed around the sphincter (Figure 6B). 16. There was some tendency for the sphincter palsy to gradually become worse. This progression was also random (Figure 8). 17. Almost all patients with Adie's syndrome had an accommodative paresis at the time of onset. 18. Reading glasses given to a patient with a fresh Adie's pupil were soon discarded as accommodation recovered (Figure 9). 19. Accomodative effort induced an astigmatism in about half of the eyes with Adie's--presumably the result of a segmental palsy of the ciliary muscle. 20. Tonicity of accommodation was present in about 1/2 of the eyes with Adie's, making it difficut for the patient to maintain a steady level of ciliary muscle tone. 21. An occasional patient complained of brow ache from ciliary spasm with near work. 22. In most patients with Adie's syndrome the ciliary muscle was supersensitive to pilocarpine 0...

Accommodation, Ocular↗

PubMed1994

Acquisition and maintenance of the simplest motor skill: investigation of CNS mechanisms.

The spinal stretch reflex (SSR), or tendon jerk, is the simplest behavior of the vertebrate nervous system. It is mediated primarily by a wholly spinal, two-neuron pathway. Recent studies from several laboratories have shown that primates, human and nonhuman, can gradually increase or decrease the size of the SSR when reward depends on such change. Evidence of this training remains in the spinal cord after all supraspinal influence is removed. Thus, the learning of this simple motor skill changes the spinal cord itself. Comparable spinal plasticity probably plays a role in the acquisition of many complex motor skills. Intracellular physiological and anatomical studies are seeking the location and nature of this spinal cord plasticity. Attention focuses on the most probable sites of change, the group Ia afferent synapse on the alpha motoneuron and the motoneuron itself. Results to date indicate that modifications are present at several places in the spinal cord. Current clinical studies are investigating the use of spinal cord adaptive plasticity as a basis for a new therapeutic approach to spasticity and other forms of abnormal spinal reflex function that result from spinal cord injury, stroke, or other neurological disorders. In the future, understanding of spinal reflex plasticity may lead to development of improved training methods for a variety of motor skills.

Adaptation, Physiological↗

PubMed1993

[Guillain-Barre syndrome: a study of 13 children].

A group of 13 children, aged 2 to 14 years, and diagnosed with Guillain-Barré syndrome has been analyzed. Clinical features and outcome were retrospectively studied. In 75% of the patients there was an infectious illness previous to the neurologic symptoms and in four children the etiologic agent was demonstrated. Motor deficits affecting the limbs and muscle stretch reflexes were absent in all thirteen patients. Cranial nerve involvement showed-up in 46%. Meningitic symptoms occurred in 62% of the cases. One of the children developed the Fisher syndrome variant. Two patients required assisted ventilation. Three children showed associated immunologic abnormalities, with one of the patients having a selective IgA deficiency, another child showing an increment in IgE and the other Kawasaki syndrome. We have not demonstrated differences in the outcome between the patients with corticoid treatment.

Adolescent↗

PubMed1993

Preprogrammed reactions in individuals with Down syndrome: the effects of instruction and predictability of the perturbation.

Preprogrammed reactions to unexpected loadings and unloadings of an elbow joint resisting an extending bias load were studied in subjects with Down syndrome. The subjects were instructed to either "let go" or "return back as fast as possible." Both predictable and unpredictable perturbation directions were used. Integrated electromyograms of the two elbow flexors and two elbow extensors were used to characterize the preprogrammed reactions. All the subjects were able to modulate their preprogrammed reactions in response to a change in the instruction. They were also able to grade the preprogrammed responses corresponding to the magnitude of the perturbation. Two basic patterns of modulation were observed, "reciprocal" and "coactivation." There were no effects of the predictability of the perturbation direction. Reconstructed joint compliant characteristics suggested an unchanged gain in the arc of the tonic stretch reflex. We propose that there are no abnormalities in the preprogrammed reactions of some individuals with Down syndrome. The apparent "clumsiness" of individuals with Down syndrome in a changing environment is assumed to reflect an adaptation to their impaired decision-making ability. The high variability of motor performance in subjects with Down syndrome may result from mixing different strategies for solving motor tasks.

Adolescent↗

PubMed1996

Electrodiagnostic evidence for cervical radiculopathy and suprascapular neuropathy in shoulder pain.

Patients diagnosed with a shoulder impingement syndrome occasionally do not respond to techniques used for treatment of soft tissue injury. The neurologic examination may be only partially abnormal or incomplete due to pain limitation so that peripheral nerve or nerve root abnormalities are overlooked. This study was undertaken to investigate the frequency of cervical radiculopathy and suprascapular neuropathy in patients with shoulder pain who were initially diagnosed with a musculoskeletal syndrome. Thirty-three subjects with a diagnosis of unilateral or bilateral impingement syndrome were entered into the study. A neurological examination was performed, followed by electromyography on 38 upper extremities and associated cervical paraspinal muscles to search for electrodiagnostic evidence for a suprascapular neuropathy and/or cervical radiculopathy. There were no subjects with electrodiagnostic evidence for suprascapular neuropathy. In two studies (5.3%), there was electrodiagnostic evidence for a C5/6 radiculopathy, and in nine (23.7%) additional subjects, there was electrodiagnostic evidence for a possible cervical radiculopathy. The remaining 27 (71.1%) studies showed no significant electrodiagnostic evidence for a cervical radiculopathy. Of the 11 subjects with abnormal electrodiagnostic studies, the neurological examination in 7 (63.6%) was normal except for pain-limited manual muscle testing, and the other 4 (36.4%) had an abnormality in either sensation testing, muscle bulk, or muscle stretch reflexes. One case of a patient with an initial diagnosis of soft tissue injury is presented. In patients undergoing evaluation for shoulder pain, cervical radiculopathy as a possible etiology should be considered, even when there is an equivocal clinical examination.

Adult↗

PubMed1996

Velocity-dependent ankle torque in the normal rat.

We evaluated the velocity-dependent ankle torque and associated activity of the ankle extensor muscle stretch reflexes in normal rats. A 287% increase in velocity-dependent ankle torque was observed at the highest velocity tested compared with the lowest velocity. Low velocity torques were minimally altered during general anesthesia that depressed EMG activity by up to 90%. However, velocity-dependent torque during higher velocity ankle rotations (306-612 degrees s-1 correlated with parallel increases in EMG magnitude recorded from the triceps surae muscles. General anesthesia (pentobarbital) abolished 61% of the velocity-dependent ankle torque at 612 degrees s-1. We conclude that ankle torque and ankle extensor muscle activity display velocity enhancement over a broad range. These observations indicate that protocols designed to assess ankle torque in the rat should use instrumentation to produce a broad range of velocities up to at least 600 degrees s-1.

Anesthesia, General↗

PubMed1997

Clinicophysiologic concepts of spasticity and motor dysfunction in adults with an upper motoneuron lesion.

Spasticity is a disorder of the sensorimotor system characterized by a velocity-dependent increase in muscle tone with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex. It is one component of the upper motoneuron syndrome, along with released flexor reflexes, weakness, and loss of dexterity. Spasticity is an important "positive" diagnostic sign of the upper motoneuron syndrome, and when it restricts motion, disability may result. The "negative" signs--weakness and loss of dexterity--invariably alter patient function when they occur. In an upper motoneuron syndrome, the alpha motoneuron pool becomes hyperexcitable at the segmental level. This hyperexcitability is hypothesized to occur through a variety of mechanisms, not all of which have yet been demonstrated in humans. Spasticity caused by spinal cord lesions is often marked by a slow increase in excitation and over-activity of both flexors and extensors with reactions possibly occurring many segments away from the stimulus. Cerebral lesions often cause rapid build-up of excitation with a bias toward involvement of antigravity muscles. Chronic spasticity can lead to changes in the rheologic properties of the involved and neighboring muscles. Stiffness, contracture, atrophy, and fibrosis may interact with pathologic regulatory mechanisms to prevent normal control of limb position and movement. In the clinical exam, it is important to distinguish between the resistance due to spasticity and that due to rheologic changes, because the distinction has therapeutic implications. Diagnostic nerve or motor point blocks and dynamic or multichannel EMG are useful to distinguish the contributions of spasticity and stiffness to the clinical problem.

Adult↗

PubMed1998

Beyond Ashworth. Electrophysiologic quantification of spasticity.

Spasticity is a hallmark of upper motor neuron lesion, which is easily identified but is difficult to quantify and treat. The Ashworth scale lacks reliability. Available biomechanical and electrophysiologic studies offer a more reliable measure of spastic hypertonia but have limited clinical utility. A uniformly acceptable, reliable, and practical measure of spasticity continues to elude the clinician. This chapter reviews the basic neuroanatomy and physiology of the stretch reflex and the pathophysiology of the spasticity. Current biomechanical and electrophysiological techniques are used to quantify spasticity.

Afferent Pathways↗

PubMed2001

A comprehensive model of spastic hypertonia derived from the pendulum test of the leg.

We propose a comprehensive model of spastic hypertonia based on clinical neurophysiology and validated using experimental data obtained from the pendulum test of the leg in 8 healthy volunteers and 15 spastic patients. This nonlinear computational model includes mechanical parameters and a stretch reflex representation involving three neural parameters: a threshold coefficient, the gain of the stretch reflex, and a time lag accounting for the reflex loop latency and the electromechanical coupling delay. Variation of the threshold coefficient alone allowed an overall reproduction of experimental data obtained from spastic and healthy subjects. We propose that this parameter could represent the supraspinal drive, supposed to be preserved in control subjects and decreased in spastic patients. No subsequent variation of the reflex gain was required to simulate spastic traces. Adjustment of the time lag influenced the duration of the swinging phase and oscillatory phenomena possibly occurring during the pendulum test. It could be related to the involvement of either short- or long-latency stretch reflex loops. With respect to current neurophysiological concepts of motor control, this modeling approach may help in understanding mechanisms underlying spastic hypertonia, and in predicting the clinical effect of antispasticity agents.

Adult↗

PubMed2001

Identification of static and dynamic components of reflex sensitivity in spastic elbow flexors using a muscle activation model.

Static and dynamic components of the stretch reflex were studied in elbow flexors of 13 hemiparetic brain-injured individuals. Constant-velocity joint rotations were applied to the elbow, and the resulting stretch reflex torque and electromyographic responses were recorded in the biceps brachii and brachioradialis muscles. Ten elbow extension velocities between 6 and 150 deg s(-1) were applied in random order. The resulting reflex torque response was plotted as a function of elbow angle and fitted with a mathematical model designed to depict elbow flexor activation. We found that four of the six model parameters were essentially independent of test velocity. Conversely, 73% (19/26) of cases involving the other two model parameters were dependent on velocity of joint extension (p<0.05). We conclude from these results that four of the model parameters reflect the static reflex response while the two remaining velocity-dependent parameters reflect the dynamic reflex response. To describe overall velocity dependence of stretch reflexes in spastic elbow muscles, the two dynamic reflex parameters were fitted to a fractional exponential function of velocity, similar to a model previously used to describe spindle firing rate in the cat hindlimb. We found that the mean velocity exponent of the dynamic reflex parameters was 0.24 + 0.17 (s.d.) (N = 13), a value similar to that for muscle spindle velocity sensitivity in reduced animal preparations. We conclude that both static and dynamic reflex sensitivities can be measured by examining different aspects of the torque/angle relation associated with the reflex response to a large-amplitude ramp stretch of the elbow.

Adult↗

PubMed2002

Muscular torque generation during imposed joint rotation: torque-angle relationships when subjects' only goal is to make a constant effort.

It is a reasonable expectation that voluntarily activated spinal motoneurons will be further excited by increases in spindle afferent activity produced by muscle stretch. Human motor behavior attributed to tonic stretch reflexes and to reflexes recruited by relatively slow joint rotation has been reported from several laboratories. We reinvestigated this issue by rotating the elbow joint over the central portion of its range while subjects focused on keeping their elbow flexion effort constant at one of three different levels and made no attempt to control the position, speed or direction of movement of their forearm. There is evidence that subjects' voluntary motor status is constant under these conditions so that any change in torque would be of involuntary origin. On average, torques rose somewhat and then fell as the elbow was flexed through a range of 80 degrees at 10, 20 and 60 degrees/s and a similar pattern occurred during elbow extension; i.e., both concentric and eccentric torque-angle profiles had roughly similar shapes and neither produced consistent stabilizing cross-range stiffness. The negative stiffness (rising torque) during the early part of a concentric movement and the negative stiffness (falling torque) during the later part of an eccentric movement would not have occurred if a stabilizing stretch reflex had been present. Positive stiffness rarely gave rise to torque changes greater than 20% in either individual or cross-subject averaged data. When angular regions of negative stiffness are combined with regions of low positive stiffness (torque change 10% or less), much of the range of motion was not well stabilized, especially during eccentric movements. The sum of the EMGs from biceps brachii, brachioradialis and brachialis showed a pattern opposite to that expected for a stretch reflex; there was an upward trend in the EMG as the elbow was flexed and a downward trend as the elbow was extended. There was little change in the shape of this EMG-angle relationship with either direction or velocity. The individual EMG-angle relationships were distinctive for each of these three elbow flexor muscles in four of the six subjects; in the remaining two, biceps was distinctive, but brachioradialis and brachialis appeared to be coupled. Although the EMGs of individual muscles were modulated over the angular range, no consistent stretch reflexes could be seen in the individual records. Thus, we could find no clear evidence for stretch reflex stabilization of human subjects maintaining a constant effort. Rather, muscle torque appears to be reflexly modulated across a much used portion of the elbow's angular range so that any appreciable stabilizing stiffness that is sustained for more than fractions of a second is associated with a change in effort.

Adult↗