Role of intracortical mechanisms in the late part of the silent period to transcranial stimulation of the human motor cortex

Transcranial magnetic stimulation (TMS) and transcranial electrical stimulation (TES) of the human motor cortex produce a silent period (SP) following motor evoked potentials (MEPs). The early part of the SP can be explained by decreased alpha motor neuron excitability, whereas the late part is presumably due to suprasegmental mechanisms. In order to determine the level of the suprasegmental contribution to the generation of SPs, we recorded excitatory and inhibitory responses to TMS, TES, and percutaneous electrical brainstem stimulation (PBS) in the voluntarily activated first dorsal interosseous muscle of the hand. Stimulus intensities were set so that PBS and TES induced MEPs with areas equal to or larger than those of MEPs obtained with TMS. This procedure revealed that SPs were 49% and 83% shorter with TES and PBS, respectively, than with TMS. As TMS is more effective than TES or PBS in activating cortical interneurons, these findings support the idea that a significant component of the SP arises from intracortical mechanisms.     

Minimizing blood transfusions during abdominal aortic surgery: recent advances in rapid autotransfusion

The purpose of this study was to determine what percentage of patients could avoid the transfusion of any homologous bank blood products during elective abdominal aortic surgery with a recently developed semicontinuous, rapid autotransfusion device. Fifty patients (26 with abdominal aortic aneurysms and 24 with aortic occlusive disease) prospectively received intraoperative autologous transfusion (group 1) and were matched for comparison with 50 patients receiving homologous blood without use of any autotransfusion equipment (group 2). For the entire perioperative period, 34 group 1 patients (68%) received only their own autotransfused blood and no other homologous blood components compared with group 2 in which 48 patients (96%) required some bank blood (p less than 0.0001). Rapid autotransfusion reduced usage of homologous red cell transfusion by 75%. The mean postoperative hemoglobin was similar in both groups (group 1, 11.91 gm/dl vs. group 2, 11.90 gm/dl, p = 0.73). Rapid autotransfusion was not associated with significant hemolysis, air embolism, or coagulopathy and did not increase morbidity or death. By eliminating the need for any bank blood components in most patients, rapid autotransfusion minimizes the risk of blood-borne diseases and transfusion reactions. New rapid autotransfusion devices offer a distinct advantage over past equipment and allow significant changes in current transfusion practices during elective abdominal aortic reconstructions.     

Physiological analysis of motor reorganization following lower limb amputation.

It is now known that amputation results in reorganization of central motor pathways, but the mechanism for the changes is unclear. One possibility is alteration of the excitability of the alpha motoneurons. We studied motor reorganization and excitability of alpha motoneurons to Ia input in 6 subjects with unilateral lower limb amputation. A Cadwell MES-10 stimulator was used to deliver transcranial magnetic stimuli through a circular coil centered on the sagittal axis 4 cm anterior to Cz and through an 8-shaped coil positioned over scalp locations 1 cm apart along the coronal axis. Surface EMG was recorded bilaterally from quadriceps femoris, the first muscle immediately proximal to the site of amputation. Excitability of the spinal alpha motoneuron pool to Ia afferents was assessed by determining the ratio of the maximal H reflex to the maximal M response (H/M ratio) elicited in the quadriceps femoris. Stimuli of equal intensity delivered to optimal scalp positions recruited a larger percentage of the alpha motoneuron pool in muscles ipsilateral to the stump than in those contralateral to the stump (P less than 0.01). Mean onset latencies of motor evoked potentials were shorter in ipsilateral muscles than in contralateral muscles (P less than 0.01). Muscles ipsilateral to the stump showed a trend toward activation from a larger number of scalp positions than those contralateral to the stump (P = 0.06). There was no difference in the quadriceps H/M ratios (7.2% ipsilateral vs. 10.9% contralateral). The absence of changes in the excitability of the alpha motoneuron pool in the presence of motor reorganization targeting muscles proximal to the stump suggests that reorganization occurs proximal to the alpha motoneuron level.     

Orbicularis oculi responses to stimulation of nerve afferents from upper and lower limbs in normal humans

A brief mechanical or electrical stimulus to peripheral nerve afferents from the upper and lower limbs elicited a small and inconsistent EMG response of the orbicularis oculi muscles. This response was facilitated when the stimuli were delivered at fixed leading time intervals, of 45–300 ms, with respect to a supraorbital nerve electrical stimulus. Also, the peripheral nerve stimulus modified the conventional blink reflex responses, inducing facilitation of R1 and inhibition of R2. These results suggest a complex processing of sensory inputs from the face and the limbs at the brainstem, where they are probably integrated in a network of interneurons influencing the excitability of facial motoneurons.     

Relevance of stimulus duration for activation of motor and sensory fibers: implications for the study of H-reflexes and magnetic stimulation.

Electric stimuli with durations of 0.5-1.0 msec are optimal for studies of H-reflexes. It is more difficult to obtain H-reflexes with shorter duration stimuli or with magnetic stimulation. In order to understand this behavior, we studied the excitation thresholds for motor and sensory fibers in the ulnar, median and tibial nerves using both electric and magnetic stimulation. For short duration electrical stimuli (0.1 msec) the threshold for motor fibers is lower than for sensory fibers. For longer duration electric stimuli (1.0 msec) the threshold for sensory fibers is lower. For magnetic stimulation the threshold for motor fibers is much lower than for sensory fibers. Thus, stimulus duration is a critical parameter for sensory fiber excitation, and current magnetic stimulators are not optimal.     

Antagonist muscle inhibition before rapid voluntary movements of the human wrist.

When a fast voluntary movement is performed from a background condition of sustained antagonist muscle activation, there is often a decrease in antagonist muscle activity before the onset of the first agonist muscle burst (AG1) that continues until the onset of the antagonist muscle burst (ANT). We studied how controlling the peak velocity, movement size, and the magnitude of antagonist muscle loading affected antagonist muscle inhibition (AntI). AntI was more pronounced during movements with lower velocity and greater size, and when performed in the direction of heavier background loads, but its variation could not be related to any single kinematic or kinetic variable in all circumstances. When AntI was larger, ANT was smaller, suggesting that AntI does not play a role similar to the premotor silence of the agonist seen before AG1 when the movement is made from a background of sustained agonist contraction. When AntI was larger, the size of AG1 was also smaller, showing that, according to the motor task, different levels of reciprocal inhibition and coactivation occur at the onset of the movement. Both AG1 and AntI produce force in the direction of the desired movement, and the central nervous system selects an appropriate balance between the two, using AntI when possible.     

The first agonist and antagonist burst in patients with an upper motor neuron syndrome

Rapid elbow flexion movements were studied in patients with an upper motor neuron syndrome following a stroke. The velocity of movements was slower than normal. The initial bursts of electromyographic (EMG) activity in both the agonist and antagonist muscles were prolonged. As in normal subjects, the first agonist burst increased in duration with larger movements, but it generally remained about 40 ms longer than normal. The size of the first agonist burst also increased with larger movements. A fixed linkage between burst duration and level of motor unit recruitment, together with a deficient corticospinal command, could explain the prolonged burst duration with preserved ability to modulate the burst.     

Etiological musculo-skeletal factor in focal dystonia in a musician's hand: A case study of the right hand of a guitarist.

A case study is presented in which a focal hand dystonia seems to have developed in the right hand of a classical guitarist as a result of a neuromuscular peripheral defect caused by trauma. The trauma was a near total perforation of the first web space by a splinter. Healing was uneventful without apparent functional complications. Two years later the patient noticed difficulties in extending the index in playing, for which he received various unsuccessful treatments during seven years. However, we found more severe dystonic symptoms (cocontractions) in the thumb than in the index during playing, which correlated with an undiagnosed insufficiency in the flexor pollicis brevis (FPB). This defect allowed proposing a biomechanical analysis of compensations for diminished thumb control in playing, which would explain the dysfunction in the index in playing as overcompensation for the thumb problem. If this analysis is correct, the etiology of the case can be traced back to underlying multiarticular control problems in the thumb caused by an insufficient FPB. This defect was considered irrepairable. It was concluded that even with knowledge of the underlying cause, a potentially successful treatment of the dystonia might not exist in this case. The case would demonstrate that task-specific hand dystonias can arise as overcompensations for (peripheral) neuro-musculoskeletal defects. The case is illustrated by videos of playing and functional thumb tests.     

Physiological abnormalities in hereditary hyperekplexia.

Five patients from a kindred with hereditary hyperekplexia had physiological testing. The surface-recorded electromyographic pattern of audiogenic muscle jerks was identical to that of the normal acoustic startle reflex. Testing at graded stimulus intensities indicated an increase in the gain of the acoustic startle reflex. Nose-tap stimuli resulted in short-latency generalized electromyographic bursts that were similar to the R1 component of the blink reflex. Electrical stimulation of peripheral nerves elicited a pattern of generalized muscle jerks that was similar to that of the acoustic startle reflex. Somatosensory evoked potentials, brainstem auditory evoked potentials, and cortical auditory evoked potentials were normal. The primary physiological abnormality in hereditary hyperekplexia is widespread elevated gain of vestigial withdrawal reflexes in the brainstem and possibly the spinal cord, most likely resulting from increased excitability of reticular neurons.