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Biomedical subjects

K H Mauritz

Publications and source records attributed to K H Mauritz.

At least 55 records · Page 3Linked to original sources
PubMed1984

A neurophysiological study of the premotor cortex in the rhesus monkey.

The frontal agranular cortex consists of at least three major subdivisions: the precentral motor cortex, the supplementary motor cortex, and the premotor cortex. Of these, the premotor cortex is by far the least intensively studied by neurophysiological methods in spite of recent evidence that it is important in higher order aspects of the cerebral control of movement ( Moll and Kuypers , 1977; Roland et al., 1980b ; Halsband and Passingham , 1982). We have accordingly studied neuronal activity in the premotor cortex of Rhesus macaques operantly conditioned to perform a visually guided motor task. We have concluded that many premotor cortex neurons appear to reflect motor set. Further, these and other premotor cortex neurons show activity patterns during and before the execution of an abstractly guided movement that are strikingly similar to what has been observed in association with movements made directly to visuospatial targets. Finally, a functional relationship of some premotor cortex unit activity to the execution of voluntary movement is supported by its close temporal correlation with the onset of movement, a significant correlation with the acceleration of the limb in some cases, and a uniform specificity for movement execution rather than the visuospatial cues that guide the movement.

Animals↗
PubMed1984

Compensation for intrinsic muscle stiffness by short-latency reflexes in human triceps surae muscles.

The incremental torque resisting rotation of the foot about the ankle joint was studied in normal seated subjects. Prior to each rotation, subjects were required to activate triceps surae (TS) muscles and maintain a constant plantar flexion torque (range 6-14 N X m) on a platform whose position was controlled by a torque motor. Subjects were instructed to increase torque as rapidly as possible once rotation commenced. Rotations ranged from 0.5 to 14 degrees amplitude and from 20 to 300 degrees/s maximum velocity. The torque in response to rotations stretching TS muscles and releasing tibialis anterior (TA) muscles increased steeply and then rapidly decreased with stretch velocity. At approximately 60 ms from stretch onset, the torque reduction terminated, torque then increased again until it began to level off at approximately 120 ms. A further large increase in torque occurred at 180 ms. A burst of short-latency (SL) electromyographic (EMG) activity in soleus (SOL) commenced at 40 ms, and was followed by a second burst at approximately 68 ms, provided that stretch deceleration started later than 20 ms after stretch onset. A period of sustained EMG activity in SOL commenced at approximately 130 ms (long-latency (LL) activity). Incremental torque in response to stretch of TA and release of TS muscles initially showed a step decrease followed by a reversal of the torque trajectory back toward base line. This change was arrested at 60 ms and torque then remained approximately constant until a large increase in torque at 180 ms. Ischemia was used to reduce SL EMG reflexes without significantly modifying the background EMG activity. A comparison between torque curves under control and ischemic conditions indicated that SL EMG activity in TS muscles recruited the force responsible for terminating the torque reduction coincident with decreasing stretch velocity. The torque response prior to the onset of force recruited by SL activity was attributed to the intrinsic properties of active muscle fibers. Thereafter, until the onset of LL activity, the torque response was attributed to intrinsic and reflex-recruited force. Torque in these two time periods was compared under a variety of stretch conditions in order to test the hypothesis that force recruited by segmental reflexes compensates for the non-linear stretch properties of active TS muscles. The relationships of SL EMG amplitudes and areas to stretch velocity and acceleration were also examined.(ABSTRACT TRUNCATED AT 400 WORDS)

Ankle Joint↗
PubMed1983

Motor aspects of cue-related neuronal activity in premotor cortex of the rhesus monkey.

Neurons in the premotor cortex of rhesus monkeys were studied under two conditions: (1) visuospatial cues were given to guide the amplitude, direction, and onset time of forearm movements or (2) physically identical visual cues were given when reward was contingent on withholding movement. Neurons with sustained activity following the cues were preferentially active when the cues triggered a movement. Thus, activity of certain neurons in this cortical field is linked to motor set, i.e. intention to make a movement in response to the cue, rather than the visual cue per se.

Animals↗
PubMed1982

Stiffness regulation provided by short-latency reflexes in human triceps surae muscles.

The triceps surae muscles of normal human subjects were rapidly stretched and released by rotating the foot about the ankle joint with a torque motor. Following the initial intrinsic resistance, the yielding observed in incremental force records was more rapid for stretch than for release responses. Short-latency EMG responses elicited by stretch recruit force, to compensate for the yielding and to maintain the total (intrinsic plus reflex) resistance constant as the prior force level changes.

Adult↗
PubMed1982

The mechanical effectiveness of short latency reflexes in human triceps surae muscles revealed by ischaemia and vibration.

The resistance to stretch provided by short latency (SL) reflexes in human triceps surae muscles was investigated under three experimental conditions: control, ischaemia, and with 100 Hz vibration applied to the Achilles tendon. Incremental changes in plantar flexion force always showed a strong initial resistance followed by yielding in response to rapid dorsiflexion of the foot about the ankle joint. These changes were attributed to inherent stiffness of the triceps surae muscles. The force curves for each experimental condition diverged during the yield phase some 20 ms after the onset of SL EMG reflexes. During ischaemia, SL EMG reflexes were reduced to 8% of control values and yielding continued until the onset of medium latency EMG activity whereas the yielding was interrupted by SL action in the control situation. The difference between the ischaemia and control force curves was attributed to force recruited by SL reflexes under normal stretch conditions. Vibration reduced the SL EMG reflex amplitude to 20% of control values and produced with it a reduced force response.

Achilles Tendon↗
PubMed1981

Delayed and enhanced long latency reflexes as the possible cause of postural tremor in late cerebellar atrophy.

The pathophysiology of postural tremor was studied in 7 patients with cortical cerebellar atrophy, and compared with the responses of 14 healthy control subjects to the same tests. Both tibial nerves were simultaneously and selectively stimulated in the fossa poplitea. EMG was recorded from agonist gastrocnemius muscles and from the antagonistic anterior tibial muscles. Displacement of the centre of foot pressure, inclination of trunk and head in the anteroposterior direction, and the ankle angle were also measured. Patients and controls both exhibit a synchronized discharge in the anterior tibial muscle (antagonist) with a latency of 120 ms to stimulus onset (tib1). Tib1 is shown to be a segmental stretch reflex elicited by the contraction of the gastrocnemius (agonist). A later, presumed long-loop response occurs after another 120 ms both in gastrocnemii and anterior tibial muscles in the normal subjects. This latency, and the amplitude of the late reflex, are increased in the patient group. The synchronization of delayed long-loop reflexes and a stretch response of the gastrocnemius in response to tib1 terminate the first cycle of the postural tremor which thereafter continues by way of the same mechanism generating a contraction of the anterior tibial muscle. Postural tremor can thus be synchronized by a single bilateral electrical stimulus and can even be elicited in incipient cases of the disease. With further progression of the cerebellar atrophy the dominant frequency of the postural tremor decreases along with an increase of long-loop latencies.

Atrophy↗
PubMed1980

[Standing ataxia in cerebellar lesions. Differential diagnosis and pathophysiology of disorders of postural control].

Several forms of postural ataxia can be distinguished in cerebellar lesions by quantitative analysis of stance, a paleocerebellar, a vestibulocerebellar and a neocerebellar syndrome, for each of which a different underlying pathomechanism was found. The pathognomonic anterior-posterior 3 Hz postural tremor in the paleocerebellar syndrome is caused by delayed and enhanced long latency reflexes, which result in an oscillation of the posture control system. In the beginning disease this oscillation can be provoked by rapid tilt or electrical stimulation of the tibial nerves. The oscillation frequency correlates inversely with the severity of the disease. In contrast to that, postural ataxia in the vestibulocerebellar syndrome is caused by a loss of intersegmental reflex patterns and a loss of the systems set value. Patients with the neocerebellar syndrome show remarkably less instability. Disturbances are often only provoked by voluntary postural movements as in tracking experiments, which suggests a defect in the interfacing of postural and voluntary motor activity. These cerebellar atactic syndromes may be separated from several forms of postural ataxias of extracerebellar origin.

Cerebellar Ataxia↗
PubMed1980

Characteristics of postural instability induced by ischemic blocking of leg afferents.

After minimizing proprioceptive input from the legs by ischemia without degradation of muscle force and excluding visual stabilization by eye closure, a characteristic anterior-posterior postural sway around 1 Hz was observed in three normal subjects. This is similar to the instability seen in two tabes dorsalis patients. From the spectral analysis of head and hip movements, displacements of the center of force and of ankle angle as well as from EMG recordings of the anterior tibial and gastrocnemius muscle it is concluded that the oscillations around 1 Hz are due to the long latency and high threshold of vestibularly induced leg muscle discharges (200-300 ms) arriving in the counterbalancing phase of the trunk, which causes an overshoot in body sway.

Adult↗
PubMed1980

Some methods and parameters of body sway quantification and their neurological applications.

Methods and parameters are described to quantify body sway as measured by a force-transducing platform. Analogue data representing the coordinates of the body's center of force (COF) are fed into a digital computer. Th following parameters are then calculated and tested for their diagnostic significance: sway path (SP), mean amplitude of sway (MA), mean sway frequency (MF), their lateral and sagittal components, and the quotients sagittal/lateral of these as well as the sway area (SA) circumscribed by the COF. Quotients of eyes open/eyes closed for all these parameters determine the visual stabilization of posture. Sway position and sway direction histograms allow for a more detailed analysis of MA and SP. Despite considerable inter- and intraindividual variance of these parameters (in 28 normals), some of them seem of clinical significance not only for documentation and follow-up studies but also for differential diagnosis. In patients with cerebellar lesions (n = 12), SP and MA were up to 10 times larger with a marked antero-posterior instability, MF being above normal. Patients with labyrinthine lesions (n = 10) showed significant instability only with eyes closed, MF being slightly below normal.

Cerebellar Ataxia↗
PubMed1980

Cyclist's palsy: Neurological and EMG study in 4 cases with distal ulnar lesions .

Four cases of cyclist's palsy -- a distal compression syndrome of the ulnar nerve which can develop after long cycling tours -- are described. In two patients extensive neurological and electromyographic (EMG) studies were performed in order to document the degree and time course of recovery of the motor and sensory deficiencies. In contrast to either EMG-studies it could be demonstrated that not only the deep motor branch of the ulnar nerve is involved, but also that a severe lesion of the superficial branch supplying the skin of the 4th and 5th finger can occur, as indicated by a complete loss of the orthodromic sensory action potential recorded above the ulnar nerve in both cases. The results furthermore show that a functionally significant paresis of the hand muscles can persist for several months. The pathogenesis and some practical implications will be discussed.

Action Potentials↗
PubMed1980

Balancing as a clinical test in the differential diagnosis of sensory-motor disorders.

During balancing on a seesaw normal individuals have a mean sway oscillation of 4.3 Hz, which is significantly lower (3.3 Hz) in patients with peroneal muscular atrophy. It is assumed that the oscillations in both cases are generated by spinal stretch reflexes and that the lower frequency in patients with peroneal muscular atrophy is due to their slower nerve conduction velocity. The balancing movements are altered when spinal stretch reflex activity is reduced by ischaemia but are normal in patients with a dorsal column lesion despite a similar sensory loss. The analysis of balancing movements can be a diagnostic tool in differentiating several sensory-motor disturbances.

Adolescent↗
PubMed1979

Quantitative analysis of stance in late cortical cerebellar atrophy of the anterior lobe and other forms of cerebellar ataxia.

(1) Methods have been developed to measure, analyse and document postural sway. The main parameters studied were: average sway amplitude; length of the sway path per unit time; sway direction and sway position histograms; and the frequency spectra of the antero-posterior and lateral sway components. (2) Postural ataxia was quantitatively studied in three groups of patients with cerebellar lesions: (a) late atrophy of the anterior lobe, (b) tumours of the cerebellar hemisphere and (c) tumours within the vestibulo-cerebellum. Characteristic differences were found. (3) Patients with anterior lobe lesion show a specific 3 Hz postural tremor in the antero-posterior direction. The tremor can be evoked by sudden destabilization in incipient cases. Less characteristic and smaller in amplitude is a mainly lateral sway component with an average frequency of 0.5 Hz. This is also seen in cases with spinal ataxia. Visual stabilization of posture is frequently preserved. Its amount does not correlate with general instability of posture. Tremor and characteristically exaggerated intersegmental responses between head, trunk, hips and legs are interpreted as the consequence of hyper-excitability of postural reflexes in these patients. (4) Patients with lesions of the hemispheres show only slight postural instability without directional preference. Their sway parameters with eyes open are within the 2 sigma range of normals and there is no significant difference from normals in these parameters even when the eyes are closed. Therefore these patients cannot be distinguished from normals by means of their platform recordings. (5) Two patients with posterior vermal and flocculo-nodular lesions were very unstable without preferred axis or frequency of instability. In contrast to the anterior lobe group the instability was characterized by the absence of intersegmental movements.

Adult↗