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Biomedical subjects

M R Dimitrijevic

Publications and source records attributed to M R Dimitrijevic.

At least 19 recordsLinked to original sources

Modification of cervical dystonia by selective sensory stimulation.

Cervical dystonia is often refractory to all forms of therapy. Many patients, however, are able to transiently abolish their spasms following a specific gesture that presumably enhances sensory input. Such observations prompted us to develop a protocol to determine if various forms of sensory stimulation could modify the motor control patterns in cervical dystonia. Surface EMG recordings of multiple neck and trunk muscles were obtained in 11 consecutive cervical dystonia patients. Baseline patterns of voluntary and involuntary muscle activation were established during a series of motor and non-motor tasks. The tasks were repeated during the application of vibratory or electrical stimulation to select muscle groups or to cutaneous and mixed nerves. Analysis of the results was made on the basis of paper and computer recordings of the data. Sensory stimulation decreased involuntary muscle activity and reduced spasms in 5 subjects. However, objective or subjective improvement usually occurred only after specific stimuli were applied to specific anatomical sites. In these cases, the protocol identified the site at which a specific sensory stimulus could be applied to control the dystonia. We conclude that selective sensory stimulation can beneficially modify cervical dystonia in some patients. Such findings warrant further investigation of the use of sensory stimulation for control of cervical dystonia.

Adult

Evidence of subclinical brain influence in clinically complete spinal cord injury: discomplete SCI.

Previous studies of the neurocontrol of movement in spinal cord injury (SCI) subjects revealed that even those without volitional movement may retain some degree of preservation of distal brain influence. We previously defined a discomplete lesion as one which is clinically complete but which is accompanied by neurophysiological evidence of residual brain influence on spinal cord function below the lesion. In order to document the nature and extent of such neurocontrol, we recorded surface EMGs from multiple muscle groups to study patterns of motor unit activity in response to tendon vibration, activation of muscles below the lesion by reinforcement maneuvers above the lesion and by voluntary suppression of plantar withdrawal reflexes. We analyzed data from this brain motor control assessment (BMCA) procedure in order to describe the frequency of occurrence and characteristics of residual control in discomplete SCI subjects, comparing with findings in (clinically and neurophysiologically) complete and in (clinically and neurophysiologically) incomplete SCI subjects. From a group of 139 SCI subjects seen for management of spasticity, 88 had clinically complete lesions. Of these, 74 (84%) were discomplete as defined by responses to the above maneuvers. The selection of management and intervention strategies, whether physiological, pharmacological, behavioral or surgical, should give consideration to the high likelihood that clinically complete subjects may be neurophysiologically incomplete.

Brain

Co-activation of ipsi- and contralateral muscle groups during contraction of ankle dorsiflexors.

Seventeen adult, healthy subjects, age 38.4 +/- 0.24 years (mean +/- SEM) 7 of which were females, were studied. Each subject was seated on a specially designed chair with trunk and legs fixed and the foot strapped to a rigid plate that was attached to a load cell. The position of the strap was adjusted so as to lie across the foot at the level of the metatarsal bones. The knee and ankle joints were adjusted to 90 degrees. To record EMG activity, pairs of surface electrodes were placed over the belly of both the right and left tibialis anterior, quadriceps, hamstring and contralateral triceps surae muscles. Two experimental paradigms were used, A and B. In A the subject was asked to sustain maximum voluntary contraction (MVC) of the ankle dorsiflexors until the force decreased to 50% of the initial value; in B the subject was asked to carry out contractions of the ankle dorsiflexors for 6 seconds followed by 4 sec relaxation periods. The initial contraction was 20% of MVC followed by 40, 60, 80 and 100% of MVC which represented one cycle. The subject was asked to repeat this cycle 10 times. Voluntary contraction of ankle dorsiflexors was regularly accompanied by activation of other muscles, usually first in the same leg, later in the contralateral leg during MVC of ankle dorsiflexors. When intermittent contractions with step wise increments of force developed by the ankle dorsiflexors were carried out, co-activation of ipsilateral and contralateral muscle groups occurred before the force of the contracting muscles decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Neurophysiological assessment of spinal cord and head injury.

Selected neurophysiologic studies can supplement clinical examination in assessing residual motor function after spinal cord or head injury. The ability of polyelectromyographic recording to detect subclinical suprasegmental control is illustrated in paraplegic patients after spinal cord injury. Excitatory or inhibitory modulation of segmental motor activity in a subpopulation of patients with clinically complete motor paralysis suggests residual connection across the lesion. This observation is consistent with the pathologic finding that complete transection of the spinal cord is rare after spinal cord injury. A preliminary study of motor-evoked potentials also indicates their potential value as an objective measure of the functional status of descending pathways. Neurophysiological assessment of subclinical residual motor function may be useful in understanding the role of suprasegmental input in the manifestation of spasticity, in objectively documenting recovery of function after injury, and may aid in the development of more specific restorative measures. Our limited experience in head-injured patients also suggests the potential usefulness of these tools in supplementing clinical evaluation.

Brain Injuries

Muscle fatigue in some neurological disorders.

Fatigue of tibialis anterior (TA) was induced by repetitive electrical stimulation. Using this test, patients with upper motor neuron muscle weakness owing to multiple sclerosis (MS) and injuries to the spinal cord showed greater fatigability of their TA muscles, suggesting that the muscle fiber population changed toward that typical of fatigable motor units. During repetitive stimulation, in addition to the decrement in tension there was an increase in half-relaxation time of tetanic contractions at 40 Hz in both subjects and patients. The increase in half relaxation during repeated activity was greater in patients with MS and spinal cord injury than in healthy subjects, suggesting that the long-term inactivity affected the efficiency of the Ca2+ uptake mechanism of their muscle fibers. Thus long-term inactivity of patients with upper motoneuron dysfunction leads to increased fatigability of their muscles and exaggerates the slowing of muscle relaxation after prolonged exercise.

Electric Stimulation

Spinal cord evoked injury potentials in patients with acute spinal cord injury.

Six patients were examined in the acute stage of spinal cord injury, between 11 h and 12 days posttrauma. Quadripolar epidural electrodes were positioned either percutaneously using a Tuohy needle or directly into the epidural space during surgical intervention. These electrodes were combined with a common reference to obtain monopolar recordings of spinal cord evoked potentials resulting from either median nerve stimulation at the wrist or tibial nerve stimulation at the popliteal fossa. Spinal cord evoked injury potentials (SCEIPs), stationary potentials with positive polarity on the distal aspect of the lesion and negative polarity on the proximal aspect, were recorded in all cases. The average amplitude (n = 3) of the SCEIP resulting from tibial nerve stimulation as measured across the lesion was 13.5 microV with an average duration of 12.7 msec. For median nerve stimulation, the average amplitude (n = 3) of the SCEIP was 16.3 microV with an average duration of 6.7 msec. There was a change in polarity in all cases over a distance of less than 6 mm, the distance between the electrode contacts on the epidural electrode. In one case, recordings were performed initially at 11 h and repeated at 21 days posttrauma. In the latter recording, the SCEIP was still present but was five times smaller in amplitude. Coincidentally, the patient also showed clinical signs of improvement in sensory and motor spinal cord function. This study demonstrates the feasibility of recording the SCEIP in patients with acute spinal cord injury, describes the features of these SCEIPs, discusses their origins, and explores the utility of recording the SCEIP as an aid in determining the severity of the injury as well as a means of monitoring changes in spinal cord function.

Action Potentials

Restorative neurology of head injury.

This article outlines the clinical characteristics of head injuries and describes their outcome. It emphasizes that some of the clinical characteristics and patterns of recovery can be explained by temporary or long-term failure in connection between different regions of the brain by specialized white matter pathways, which results in so-called dysconnection syndromes. It points out that the ability to assess these dysconnection syndromes leads to the prevention of disuse of the uninjured part of the brain and suppression of secondary brain dysfunctions. The second part of this article describes restorative neurology and then discusses how it is becoming possible to breach the existing gap between cellular and human holistic neurobiology. It concludes that restorative neurology research programs will be used routinely in the treatment of patients with acute and chronic head injury.

Craniocerebral Trauma

Direct spinal effect of a benzodiazepine (midazolam) on spasticity in man.

The water-soluble benzodiazepine, midazolam, was administered epidurally over the lumbar enlargement 18 times to 9 patients with spasticity due to severe spinal cord injury. Doses of 1.25-3.75 mg produced a rapid decrease of spasticity which lasted 1 h. After the maximal reduction of spasticity, the patients became drowsy. While the results suggest a direct action of midazolam on the spinal cord to reduce spasticity, the effect does not contribute to its usefulness as a therapeutic tool.

Adult

Model for the study of plasticity of the human nervous system: features of residual spinal cord motor activity resulting from established post-traumatic injury.

Established post-traumatic spinal cord injuries can serve as an 'experimental model' in which trauma has partially separated the 'spinal neuronal pool' from supraspinal influence. Our findings show that: (1) when the muscle is deprived of upper motor neuron activity, fatigue resistance is diminished and external, electrically induced daily contractions will restore the level of fatigue resistance close to that of muscles in healthy, active subjects; (2) the spinal interneuron network, when completely deprived of brain influence, is a 'spinal reflex centre' with a relatively restricted and low excitability level; and (3) the 'discomplete spinal cord injury' model illustrates that spasticity is of supra-segmental origin and that there are two basic features of brain motor control of the spinal interneuron system: the command to restrict interneuronal pool activity and the command to activate the interneuronal network. Moreover, I have described the modifiability of fatigue resistance, locomotor patterns and different alternatives in the neurocontrol of motor activity, depending on the kind and degree of residual brain influence. Such significant modifiability can be thought of as plasticity of the neuromuscular system and impaired control of the nervous system.

Humans

Restorative neurology of progressive neuromuscular disorders.

Patients with progressive neuromuscular diseases (PND) suffer from motor disabilities which result not only from muscle weaknesses but also from the response of the upper motor neuron to these weaknesses. A short review of studies of the neurocontrol of posture and gait is given for patients with PND and their importance for the maintenance of ambulation will be reviewed. It is proposed that the newly established procedures for the modification of muscle properties by means of low frequency stimulation can further restore motor activities when used in conjunction with motor studies soon after the onset of PND.

Electric Stimulation Therapy

Voluntary supraspinal suppression of spinal reflex activity in paralyzed muscles of spinal cord injury patients.

Having previously demonstrated that residual facilitatory brain influence on segmental structures occurs in paralyzed spinal cord injury patients, we sought evidence of suprasegmental suppression in such patients. By recording EMG activity from leg muscles, we studied changes in segmental excitability of the plantar reflex elicited by cutaneous stimulation of the plantar surface. Using surface EMG recordings, 50 paralyzed spinal cord injury patients were examined for their ability to volitionally suppress the plantar reflex on three repeated trials after three baseline trials. The patients, who had no voluntary EMG activity in the monitored muscles, were able to volitionally suppress the plantar reflex responses by 45% in the tibialis anterior, hamstring, and triceps surae muscles and to suppress the quadriceps response by 72%. In this patient group, 73 of 100 tibialis anterior muscle groups showed suppression of more than 20% compared with the control response. On reexamination, these findings were consistent during a period of 2 years in six patients. We conclude that suprasegmental suppression of segmental activity does occur in paralyzed spinal cord injury patients, and that in clinically complete patients, neurological evaluation should include assessment of the degree of preservation of suprasegmental neurocontrol on segmental activity below the lesion.

Adolescent