Patterned ballistic movements triggered by a startle in healthy humans.
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1. The reaction time to a visual stimulus shortens significantly when an unexpected acoustic startle is delivered together with the 'go' signal in healthy human subjects. In this paper we have investigated the physiological mechanisms underlying this effect. If the commands for the startle and the voluntary reaction were superimposed at some level in the CNS, then we would expect to see alterations in the configuration of the voluntary response. Conversely, if the circuit activated by the startling stimulus is somehow involved in the execution of voluntary movements, then reaction time would be sped up but the configuration of the motor programme would be preserved. 2. Fourteen healthy male and female volunteers were instructed to react as fast as possible to a visual 'go' signal by flexing or extending their wrist, or rising onto tiptoe from a standing position. These movements generated consistent and characteristic patterns of EMG activation. In random trials, the 'go' signal was accompanied by a very loud acoustic stimulus. This stimulus was sufficient to produce a startle reflex when given unexpectedly on its own. 3. The startling stimulus almost halved the latency of the voluntary response but did not change the configuration of the EMG pattern in either the arm or the leg. In some subjects the reaction times were shorter than the calculated minimum time for processing of sensory information at the cerebral cortex. Most subjects reported that the very rapid responses were produced by something other than their own will. 4. We conclude that the very short reaction times were not produced by an early startle reflex adding on to a later voluntary response. This would have changed the form of the EMG pattern associated with the voluntary response. Instead, we suggest that such rapid reactions were triggered entirely by activity at subcortical levels, probably involving the startle circuit. 5. The implication is that instructions for voluntary movement can in some circumstances be stored and released from subcortical structures. (+info)
Contact-evoked changes in EMG activity during human grasp.
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Contact-evoked changes in EMG activity during human grasp. 2215 Cutaneous receptors in the digits discharge bursts of activity on contact with an object during human grasp. In this study, we investigated the contribution of this sensory activity to the responses of muscles involved in the task. Twelve subjects performed a standardized precision grasp task without the aid of vision. Electromyographic (EMG) responses in trials when the object was present were compared with those in which the object, and hence the associated afferent responses, were unexpectedly absent. Significant differences in EMG amplitude occurred in the interval 50-100 ms after contact in all subjects and in 33/46 of the muscles sampled. The differences emerged as early as 34 ms after contact and comprised as much as a fourfold change in EMG from 50 to 100 ms after contact with the object. Typically, EMG responses were larger when the object was present (OP), though there were cases, particularly in the thenar muscles, in which the responses increased when the object was absent (OA). Local anesthesia of the thumb and index finger attenuated contact-evoked EMG activity in at least one muscle in all four subjects tested. In one subject, contact-evoked responses were abolished completely during the anesthesia in all four muscles sampled. The results indicate that the sensory activity signaling contact plays a key role in regulating EMG activity during human grasp. Much of this feedback action is attributable to cutaneous receptors in the digits and probably involves both spinal and supraspinal pathways. (+info)
Conduction block in carpal tunnel syndrome.
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Wrist extension was performed in six healthy subjects to establish, first, whether it would be sufficient to produce conduction block and, secondly, whether the excitability changes associated with this manoeuvre are similar to those produced by focal nerve compression. During maintained wrist extension to 90 degrees, all subjects developed conduction block in cutaneous afferents distal to the wrist, with a marked reduction in amplitude of the maximal potential by >50%. This was associated with changes in axonal excitability at the wrist: a prolongation in latency, a decrease in supernormality and an increase in refractoriness. These changes indicate axonal depolarization. Similar studies were then performed in seven patients with carpal tunnel syndrome. The patients developed conduction block, again with evidence of axonal depolarization prior to block. Mild paraesthesiae were reported by all subjects (normals and patients) during wrist extension, and more intense paraesthesiae were reported following the release of wrist extension. In separate experiments, conduction block was produced by ischaemic compression, but its development could not be altered by hyperpolarizing currents. It is concluded that wrist extension produces a 'depolarization' block in both normal subjects and patients with carpal tunnel syndrome, much as occurs with ischaemic compression, but that this block cannot be altered merely by compensating for the axonal depolarization. It is argued that conduction slowing need not always be attributed to disturbed myelination, and that ischaemic compression may be sufficient to explain some of the intermittent symptoms and electrodiagnostic findings in patients with carpal tunnel syndrome, particularly when it is of mild or moderate severity. (+info)
Sonographic features of fetal trisomy 18 at 13 and 14 weeks: four case reports.
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Fetal trisomy 18 is the second most common multiple malformation syndrome. We present four cases of trisomy 18 with multiple sonographic abnormalities at 13 and 14 weeks of gestation. These cases demonstrated that fetal hand deformities can be a tell-tale sign of trisomy 18 with or without increased nuchal translucency at this gestation. (+info)
A double-blind, placebo-controlled investigation of the effects of fexofenadine, loratadine and promethazine on cognitive and psychomotor function.
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AIMS: To assess whether fexofenadine in a range of doses from 80 to 180 mg has any disruptive effects on aspects of psychomotor and cognitive function in comparison with placebo, loratadine and promethazine, an antihistamine known to produce psychomotor and cognitive impairment. METHODS: Twenty-four healthy volunteers received fexofenadine 80 mg, 120 mg and 180 mg, loratadine 10 mg, promethazine 30 mg (as a positive internal control) and placebo in a six-way crossover, double-blind study. Following each dose, subjects were required to perform a series of tests of cognitive function and psychomotor performance at 1.5, 3, 6, 9, 12 and 24 h post dose. The test battery included critical flicker fusion (CFF), choice reaction time (CRT) and assessment of subjective sedation (LARS). Overall levels of activity were monitored by means of wrist mounted actigraphs throughout each of the 24 h experimental periods. RESULTS: Fexofenadine at all doses tested was not statistically different from placebo in any of the tests used and loratadine did not cause any significant impairment of cognitive function. Significant impairments were found following promethazine. Promethazine caused a significant reduction in CFF threshold and this effect was evident up to 12 h post dose (P<0.05). There was a significant increase in recognition reaction time at 3 and 6 h post promethazine administration, and the drug caused a significant (P<0. 002) increase in the percentage of 'sleep-like' activity from actigraph records during the daytime. CONCLUSIONS: Fexofenadine at doses up to 180 mg appears free from disruptive effects on aspects of psychomotor and cognitive function in a study where the psychometric assessments have been shown to be sensitive to impairment, as evidenced by the effects of the verum control promethazine 30 mg. (+info)
Dissociation of the pathways mediating ipsilateral and contralateral motor-evoked potentials in human hand and arm muscles.
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1. Growing evidence points toward involvement of the human motor cortex in the control of the ipsilateral hand. We used focal transcranial magnetic stimulation (TMS) to examine the pathways of these ipsilateral motor effects. 2. Ipsilateral motor-evoked potentials (MEPs) were obtained in hand and arm muscles of all 10 healthy adult subjects tested. They occurred in the finger and wrist extensors and the biceps, but no response or inhibitory responses were observed in the opponens pollicis, finger and wrist flexors and the triceps. 3. The production of ipsilateral MEPs required contraction of the target muscle. The threshold TMS intensity for ipsilateral MEPs was on average 1.8 times higher, and the onset was 5.7 ms later (in the wrist extensor muscles) compared with size-matched contralateral MEPs. 4. The corticofugal pathways of ipsilateral and contralateral MEPs could be dissociated through differences in cortical map location and preferred stimulating current direction. 5. Both ipsi- and contralateral MEPs in the wrist extensors increased with lateral head rotation toward, and decreased with head rotation away from, the side of the TMS, suggesting a privileged input of the asymmetrical tonic neck reflex to the pathway of the ipsilateral MEP. 6. Large ipsilateral MEPs were obtained in a patient with complete agenesis of the corpus callosum. 7. The dissociation of the pathways for ipsilateral and contralateral MEPs indicates that corticofugal motor fibres other than the fast-conducting crossed corticomotoneuronal system can be activated by TMS. Our data suggest an ipsilateral oligosynaptic pathway, such as a corticoreticulospinal or a corticopropriospinal projection as the route for the ipsilateral MEP. Other pathways, such as branching of corticomotoneuronal axons, a transcallosal projection or a slow-conducting monosynaptic ipsilateral pathway are very unlikely or can be excluded. (+info)
Estrogen supplementation for bone dematuration in young epileptic man treated with anticonvulsant therapy; a case report.
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We encountered a young man treated with anticonvulsant therapy who had greatly reduced bone mineral density. An 18-year-old man was admitted to our hospital for shoulder pain and further evaluation of decreased bone mineral density. He had been treated with anticonvulsants, including phenytoin, phenobarbital, valproic acid and zonisamide for seizures. Although testosterone was found within the normal range for adult men, the serum estrogen concentration was below the detection limit (< 10 pg/ml) and his wrist epiphyses were not yet closed. After 10 months of treatment with the conjugated estrogen, both his height and weight showed improvement, while his bone mineral density and bone age were increased. These findings suggested that estrogen therapy had a significant effect on his skeletal growth and bone maturation in man. This is the first report showing the beneficial effect of estrogen supplementation in an epileptic man receiving treatment with anticonvulsants. (+info)
Muscle and movement representations in the primary motor cortex.
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What aspects of movement are represented in the primary motor cortex (M1): relatively low-level parameters like muscle force, or more abstract parameters like handpath? To examine this issue, the activity of neurons in M1 was recorded in a monkey trained to perform a task that dissociates three major variables of wrist movement: muscle activity, direction of movement at the wrist joint, and direction of movement in space. A substantial group of neurons in M1 (28 out of 88) displayed changes in activity that were muscle-like. Unexpectedly, an even larger group of neurons in M1 (44 out of 88) displayed changes in activity that were related to the direction of wrist movement in space independent of the pattern of muscle activity that generated the movement. Thus, both "muscles" and "movements" appear to be strongly represented in M1. (+info)