SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
These recommendations are presented to enhance the safety and efficacy of AEDs intended for public access. The task force recommends that manufacturers present developmental and validation data on their own devices, emphasizing high sensitivity for shockable rhythms and high specificity for nonshockable rhythms. Alternative defibrillation waveforms may reduce energy requirements, reducing the size and weight of the device. The highest levels of safety for public access defibrillation are needed. Safe and effective use of AEDs that are widely available and easily handled by non-medical personnel has the potential to dramatically increase survival from cardiac arrest.
The law on automatism is undergoing change. For some time there has been a conflict between the medical and the legal views. The medical profession believes that the present division between sane and insane automatism makes little medical sense. Insane automatism is due to an internal factor, that is, a disease of the brain, while sane automatism is due to an external factor, such as a blow on the head or an injection of a drug. This leads to the situation where, for example, the hypoglycaemia resulting from injected insulin would be sane automatism, while hypoglycaemia while results from an islet tumour would be insane automatism. This would not matter if the consequences were the same. However, sane automatism leads to an acquittal, whereas insane automatism leads to committal to a secure mental hospital. This article traces the development of the concept of automatism in the 1950s to the present time, and looks at the anomalies in the law as it now stands. It considers the medical conditions of, and the law relating to, epilepsy, alcohol and drug automatism, hypoglycaemic automatisms, transient global amnesia, and hysterical automatisms. Sleep automatisms, and offences committed during a somnambulistic automatism, are also discussed in detail. The article also examines the need of the Courts to be provided with expert evidence and the role that the qualified medical practitioner should take. It clarifies the various points which medical practitioners should consider when assessing whether a defence of automatism is justified on medical grounds, and in seeking to establish such a defence. The present law is unsatisfactory, as it does not allow any discretion in sentencing on the part of the judge once a verdict of not guilty by virtue of insane automatism has been passed. The judge must sentence the defendant to detention in a secure mental hospital. This would certainly be satisfactory where violent crimes have been committed. However, it is inappropriate in many cases where non-violent confusional crimes, such as petty larceny, have been committed. Suggestions are made for desirable changes in the law.
Patients with Parkinson's disease have great difficulty performing learned movements automatically. The neural contribution to the problem has not been identified. In the current study, we used functional magnetic resonance imaging (fMRI) to investigate the underlying neural mechanisms of movement automaticity in Parkinson's disease patients. Fifteen patients with Parkinson's disease were recruited. Three patients were finally excluded because they could not achieve automaticity. The remaining 12 patients were aged from 52 to 67 years, with a mean age of 61.2 years. Controls included 14 age-matched normal subjects. The subjects were asked to practise four tasks, including two self-initiated, self-paced sequences of finger movements with different complexity until they could perform the tasks automatically. Two dual tasks were used to evaluate automaticity. For dual tasks, subjects performed a visual letter-counting task simultaneously with the sequential movements. Twelve normal subjects performed all sequences automatically. All patients performed sequences correctly; 12 patients could perform the simpler sequence automatically; and only 3 patients could perform the more complex sequence automatically. fMRI results showed that for both groups, sequential movements activated similar brain regions before and after automaticity was achieved. No additional activity was observed in the automatic condition. In normal subjects, many areas had reduced activity at the automatic stage, whereas in patients, only the bilateral superior parietal lobes and left insular cortex were less activated. Patients had greater activity in the cerebellum, premotor area, parietal cortex, precuneus and prefrontal cortex compared with normal subjects while performing automatic movements. We conclude that Parkinson's disease patients can achieve automaticity after proper training, but with more difficulty. Our study is the first to demonstrate that patients with Parkinson's disease require more brain activity to compensate for basal ganglia dysfunction in order to perform automatic movements.
There is evidence that aged normal subjects have more difficulty in achieving automaticity than young subjects. The underlying central neural mechanism for this phenomenon is unclear. In the present study, functional magnetic resonance imaging (fMRI) was used to investigate the effect of normal ageing on automaticity. Aged healthy subjects were asked to practice self-initiated, self-paced, memorized sequential finger movements with different complexity until they could perform the tasks automatically. Automaticity was evaluated by having subjects perform a secondary task simultaneously with the sequential movements. Although it took more time, most aged subjects eventually performed the tasks automatically at the same level as the young subjects. Functional MRI results showed that, for both groups, sequential movements activated similar brain regions before and after automaticity was achieved. No additional activity was observed in the automatic condition. While performing automatic movements, aged subjects had greater activity in the bilateral anterior lobe of cerebellum, premotor area, parietal cortex, left prefrontal cortex, anterior cingulate, caudate nucleus and thalamus, and recruited more areas, including the pre-supplementary motor area and the bilateral posterior lobe of cerebellum, compared to young subjects. These results indicate that most healthy aged subjects can perform some complex motor tasks automatically. However, aged subjects appear to require more brain activity to perform automatically at the same level as young subjects. This appears to be the main reason why aged subjects have more difficulty in achieving automaticity.
Fifty percent of adult canine Purkinje fibers manifest a decrease in automaticity in response to alpha 1-adrenergic stimulation with 10(-10)-10(-8) M norepinephrine (NE), and 50% manifest an increase. In contrast, most neonatal Purkinje fibers show an increase in automaticity in response to these concentrations of NE. We studied the modulation of NE effects, using the subtype selective alpha 1-adrenergic antagonists chloroethylclonidine (CEC) and WB 4101. CEC selectively antagonized the decrease in automatically such that, in both age groups, all Purkinje fibers showed NE-induced increases in automaticity. In Purkinje fibers from dogs treated with pertussis toxin, NE no longer induced a CEC-sensitive decrease in automaticity. In contrast, WB 4101 selectively antagonized the NE-induced increase in automaticity in both age groups. In the presence of WB 4101, NE decreased automaticity uniformly in adult Purkinje fibers and tended to induce no change in automaticity in neonatal Purkinje fibers. In the presence of prazosin (10(-6) M) or combined CEC (10(-7) M) and WB 4101 (10(-7) M), no alpha-agonist-induced increase or decrease in rate was observed. Pretreatment of membranes from newborn and adult dog and rat ventricles with CEC resulted in a selective and irreversible inactivation of 25% of specific binding sites labeled with [125I]IBE2254. In cultured neonatal rat ventricular myocytes, exposure to CEC resulted in a 35% decrease in the density of specific binding sites labeled with [125I]IBE2254 but did not influence alpha-adrenergic stimulation of inositol phosphate accumulation. In contrast, WB 4101 inactivated NE-stimulated inositol phosphate accumulation. Our results suggest that 1) at least two distinct alpha 1-adrenergic receptor subtypes are present in neonatal and adult cardiac tissue, 2) the CEC-sensitive subtype is linked to a decrease in automaticity via a pertussis toxin-sensitive substrate, 3) the WB 4101-sensitive subtype is linked to an increase in automaticity (possibly via a mechanism related to phosphoinositide breakdown), and 4) although CEC- and WB 4101-sensitive alpha 1-adrenergic receptor subtypes are present in the neonate, only the WB 4101-sensitive subtype is expressed functionally to induce effects on ventricular automaticity.
PURPOSE: To describe clinical characteristics and lateralizing value of postictal automatisms in patients with temporal lobe epilepsy (TLE). METHODS: One hundred and ninety-three videotaped seizures of 55 consecutive patients with refractory TLE and postoperatively seizure-free outcome were analyzed. Ictal as well as postictal (manual, oral and speech) automatisms were monitored. RESULTS: Thirty-four (62%) of the 55 patients showed PA at least once during their seizures. Postictal automatism was observed in 70 (36%) attacks as manual (21%), oral (13%) or speech (9%) automatisms. Fifteen seizures contained a combination of two different postictal automatisms. The presence of postictal oral automatisms did not lateralize the seizure onset zone (p=0.834). Speech automatisms (repetitive verbal behavior) occurred more frequently after left-sided seizures (p=0.002). Postictal unilateral manual automatism showed no lateralizing value occurring by the ipsilateral hand in 10 and the contralateral upper limb in 6 seizures (p=0.454). CONCLUSION: : Postictal automatism is a relatively frequent phenomenon in TLE. Postictal speech automatism lateralizes the seizure onset zone to the left hemisphere. Our observation can help the presurgical evaluation of TLE because verbal perseveration frequently occurs spontaneously, even in seizures without appropriate postictal language testing.
We used functional magnetic resonance imaging (fMRI) and dual tasks to investigate the physiology of how movements become automatic. Normal subjects were asked to practice some self-initiated, self-paced, memorized sequential finger movements with different complexity until they could perform the tasks automatically. Automaticity was evaluated by having subjects perform a secondary task simultaneously with the sequential movements. Our secondary task was a letter-counting task where subjects were asked to identify the number of times a target letter from the letter sequences was seen. Only the performances that achieved high accuracy in both single and dual tasks were considered automatic. The fMRI results before and after automaticity was achieved were compared. Our data showed that for both conditions, sequential movements activated similar brain regions. No additional activity was observed in the automatic condition. There was less activity in bilateral cerebellum, presupplementary motor area, cingulate cortex, left caudate nucleus, premotor cortex, parietal cortex, and prefrontal cortex during the automatic stage. These findings suggest that most of the motor network participates in executing automatic movements and that it becomes more efficient as movements become more automatic. Our results do not provide evidence for any area to become more activated for automatic movements.
It is unknown to what extent automatic postural responses are triggered by lower leg proprioception. This issue was addressed by studying postural control in five carefully selected patients with subtle diabetic polyneuropathy (restricted to the lower legs) and 15 healthy subjects. All patients had bilaterally absent Achilles tendon reflexes and weak or absent patella tendon reflexes, but muscle strength was fully preserved. Subjects were tested while standing on a supporting, movable force-plate. The contribution of lower leg proprioception to automatic postural responses was investigated by randomly exposing the subjects to either a 4 degrees 'toe-up' rotational perturbation ('normal ankle input'), a simultaneous 4-cm rearward translation and 4 degrees toe-up rotation ('enhanced ankle input'), or a simultaneous 4-cm rearward translation and 4 degrees 'toe-down' rotation ('nulled ankle input'). We recorded surface EMG (stretch reflexes and balance-correcting responses) from leg and trunk muscles, ankle torque and angular velocities of the upper and lower legs and trunk. We argued that automatic postural responses that have abnormally small amplitudes in patients and are modulated in controls with the velocity of different types of ankle rotations must receive a major input from lower leg proprioception. Conversely, automatic postural responses that are weakly modified in amplitude or onset by different ankle perturbations and are present despite nulled ankle inputs and, finally, are unaffected in patients with distal polyneuropathy must be triggered or modulated by inputs other than from lower leg proprioception. Normal postural synergies and strategies were maintained in patients, although within a given synergy the timing and amplitude of some automatic postural responses were abnormal. A few automatic postural responses appeared to be triggered or modulated by lower leg proprioception. Thus, early stretch reflexes in soleus and medial gastrocnemius were severely diminished in patients, while in controls these stretch reflexes were modulated by different ankle perturbations. Furthermore, balance-correcting responses in tibialis anterior were diminished and delayed in patients, while in controls these balance-correcting responses were modulated by different ankle perturbations. Other automatic postural responses were apparently not triggered or modulated by lower leg proprioception, but likely received a major input from more proximal sensory systems. Thus, in both groups prominent balance-correcting responses were present in several muscles (soleus, gastrocnemius, quadriceps, paraspinals and trapezius) during the 'nulled ankle input' condition, where ankle position was stabilised over the first 250 ms. During the 'enhanced ankle input' condition, where prominent ankle dorsiflexion occurred during the first 200 ms, amplitudes of balance-correcting responses were only marginally weaker in patients than in controls. We analysed body segment displacements to unveil the potential nature of proximal triggers for automatic postural responses. As opposed to the 'inverted pendulum' concept of postural control, early movement occurred in the knees, hips and trunk well before the onset of automatic postural responses. For example, during the 'nulled ankle input' condition, the lower leg moved forward with early knee flexion, followed by knee extension. The trunk extended backwards at 80 ms, which was followed by forward flexion. The absent stretch reflex and weaker balance-correcting responses in patients produced changed trunk velocity profiles (mainly a reduced initial backward motion of the trunk), but lower-body segment movements showed no consistent differences between the two groups. Considering these body segment displacements, any automatic postural response with an onset within the first 200 ms could well be triggered by receptors located at the knee, hip or trunk. (ABSTRACT TRUNCATED)
INTRODUCTION: Automatic rhythms associated with Mahaim fibers usually occur during radiofrequency catheter ablation. The incidence and significance of spontaneous automaticity in Mahaim fibers are unknown. METHODS AND RESULTS: Spontaneous automatic rhythms were observed in 5 (12.5%) of 40 patients with Mahaim fibers referred for nonpharmacologic therapy because of recurrent episodes of symptomatic tachyarrhythmias, usually antidromic circus movement tachycardia (33/40 patients). Three were female and two were male. Their mean age was 15 +/- 7 years compared to 26 +/- 13 years of the patients without automaticity (P = 0.09). Three patients had both antidromic tachycardia and asymptomatic spontaneous automatic rhythms recorded during ambulatory ECG (1 patient) or electrophysiologic study (2 patients). In 2 patients, the automatic rhythm triggered antidromic tachycardia. Two other patients had nonsustained repetitive episodes of wide QRS tachycardia due to automaticity arising in the Mahaim fiber, without antidromic tachycardia. All automatic rhythms were abolished by successful catheter ablation of the Mahaim fibers. CONCLUSION: Spontaneous automaticity occurred in 12.5% of our Mahaim patients and may trigger antidromic tachycardia. Spontaneous automaticity, which is not seen in rapidly conducting accessory pathways, is another argument for the presence of an AV nodal-like structure in Mahaim fibers.
The effect of adenosine and its analogues, 5'-N-ethyl-carboxamide adenosine (NECA), L-N6-phenylisopropyladenosine (L-PIA) and 2-chloroadenosine (CADO) on ventricular automaticity induced by a local injury, has been studied in the isolated right ventricle of the rat. Adenosine had both excitatory and inhibitory actions on ventricular automaticity, the excitatory action being observed with lower concentrations of adenosine. The adenosine analogues NECA and CADO, mimicked the excitatory action of adenosine on ventricular automaticity, with NECA being much more potent than CADO. NECA and CADO also had inhibitory effects on ventricular automaticity, with CADO being more potent than NECA. L-PIA only caused inhibitory effects on ventricular automaticity. In reserpinized animals, adenosine did not cause any excitatory effect on ventricular automaticity, and the inhibitory action of adenosine was potentiated. In the presence of propranolol, adenosine also did not exhibit its excitatory effect on ventricular automaticity. In reserpinized rats, noradrenaline restored the excitatory action of adenosine on ventricular automaticity. In the presence of dibutyryl cyclic AMP, adenosine only caused excitatory effects on ventricular automaticity in reserpinized rats. The results suggest the involvement of catecholamines in the excitatory action of adenosine on ventricular automaticity, an effect probably linked to accumulation of intracellular cyclic AMP.
CONTEXT: Approximately 10 million cars with automatic shoulder belt systems are currently in use in the United States. However, reports on the effectiveness of such restraints have yielded conflicting results. OBJECTIVE: To determine the effectiveness of automatic shoulder belt systems in reducing the risk of injury and death among front-seat passenger vehicle occupants. DESIGN, SETTING, AND SUBJECTS: Analysis of data collected from the 1993-1996 National Highway Traffic Safety Administration Crashworthiness Data System on front-seat occupants involved in 25,811 tow-away crashes of passenger cars, light trucks, vans, and sport utility vehicles. MAIN OUTCOME MEASURES: Death and serious injury to specific body areas by use of manual lap and shoulder belts, automatic shoulder belts with manual lap belts, or automatic shoulder belts without lap belts, compared with no restraint use. RESULTS: Use of automatic shoulder belts without lap belts was associated with a decrease in the risk of death vs no restraint use but was not statistically significant for all crashes (odds ratio [OR], 0.66; 95% confidence interval [CI], 0.42-1.06) or for frontal crashes (OR, 0.71; 95% CI, 0.38-1.35) after adjustment for occupant age, sex, vehicle year, air-bag deployment, estimated change in vehicle speed during the crash, and principal direction of force. This association was significantly weaker than the 86% lower risk observed for use of automatic shoulder belts with lap belts (OR, 0.14; 95% CI, 0.07-0.26 vs no restraint; P<.05). Use of automatic shoulder belts without lap belts was associated with an increased risk of serious chest (OR, 2.66; 95% CI, 1.11-6.35) and abdominal (OR, 2.06; 95% CI, 1.004-4.22) injuries for all crashes. CONCLUSIONS: These data indicate that improperly used automatic restraint systems may be less effective than properly used systems and are associated with an increased risk of serious chest and abdominal injuries. Given the continued widespread use of these automatic systems, educational programs may be warranted. JAMA. 2000;283:2826-2828
The capability of generating spontaneous diastolic depolarization and automaticity was investigated in vitro by means of standard microelectrode techniques in 50 human atrial preparations. Samples were classified within two groups: group 1 was composed of 12 well-polarized preparations exhibiting action potentials that were fast responses (mean maximum diastolic potential: -75.5 mV and Vmax greater than 100 V/s); group 2 was composed of 38 partially-depolarized samples (mean maximum diastolic potential: -50.3 mV and Vmax less than 10 V/s) and was further divided into two subgroups. Subgroup 2A consisted of 20 spontaneously beating preparations and subgroup 2B consisted of 18 non-automatic partially-depolarized specimens. Highly-polarized fibers from group 1, although exhibiting a slight diastolic depolarization which was almost entirely suppressed by 2 mM caesium, never presented spontaneous activity under our experimental conditions. 90% of automatic fibers from subgroup 2A were sampled from dilated atria. In automatic preparations, diastolic depolarization was usually separated into two phases: an initial phase, also present in non-automatic fibers, and a late phase. Changes in the initial phase were not accompanied by concomitant changes in the spontaneous rate. Abnormal automaticity was clearly related to the late diastolic phase (absent in non-automatic fibers), the generation of which appeared to be a specific property of automatic fibers. The use of K conductance inhibitors (caesium, 4-aminopyridine, barium, low K solutions) provided indirect evidence that neither delayed outward ix current nor if type inward current are principally responsible for abnormal automaticity.
The aim of this study was to compare measurements of echocardiographic volume with an on-line automatic boundary detection imaging system with those of a conventional off-line method for routine clinical studies. Automatic boundary detection imaging shows promise as a rapid, on-line method for quantitating left ventricular volumes by echocardiography. However, there is little information about the role of automatic boundary detection for routine clinical studies. Ninety-seven patients with a variety of clinical diseases who were referred for clinical transthoracic echocardiographic evaluation were studied in apical four-chamber and two-chamber imaging planes. End-diastolic volume, end-systolic volume, and ejection fraction obtained with automatic boundary detection images were compared with those of conventional off-line analysis. Segmental endocardial definition and border tracking were evaluated on all automatic boundary detection images. Left ventricular end-diastolic volumes obtained by automatic boundary detection correlated well but were systematically under-estimated compared with off-line analysis for the apical two-chamber (r = 0.83; underestimation = 42 +/- 33 ml; p < 0.05) and four-chamber views (r = 0.83; underestimation = 43 +/- 31 ml; p < 0.05). Left ventricular end-systolic volumes also correlated well but were underestimated by automatic boundary detection for the apical two-chamber (r = 0.83; underestimation = 14 +/- 26 ml; p < 0.05) and four-chamber views (r = 0.83; underestimation = 18 +/- 24 ml; p < 0.05). Ejection fraction was not predicted accurately for the entire study population (n = 97). However, for patients with complete endocardial definition (n = 32), automatic boundary detection accurately predicted ejection fraction with no systematic error compared with manually traced images for both the apical two-chamber (r = 0.86; p < 0.05) and four-chamber (r = 0.82; p < 0.05) views. Segmental analysis of endocardial tracking revealed significantly better tracking of the septal and lateral walls compared with other regions (p < 0.05). End-diastolic and end-systolic volumes determined by automatic boundary detection correlate well but underestimate volume compared with conventional off-line analysis. However, ejection fraction compares favorably for the two methods when there is complete endocardial definition.
The interrelationship between drug-induced changes in heart rate and drug-induced alterations in ventricular automaticity was studied in dogs with intact conduction systems and dogs with surgically-induced complete heart block. The effects of epinephrine (0.5 microgram-kg-1-min-1) and propranolol (1.0 mg-kg-1) on ventricular automaticity were shown to be partially concealed by heart rate changes produced by these agents. Partial concealment of ventricular automaticity changes was shown to result from an alteration in the degree of overdrive suppression secondary to rate changes. Changes in the degree of overdrive suppression have a masking effect on drug-induced alterations in ventricular automaticity and only when the degree of suppression was held constant could the full extent of drug effects on ventricular automaticity be determined. Following vagal stimulation or rapid pacing, the rate of recovery from overdrive suppression as measured by the number of ventricular beats in 30 s was shown to be a dependable index of ventricular automaticity. It was concluded that determinations of drug effects on ventricular automaticity should take into account changes in heart rate produced by the drug. A method for determining ventricular automaticity is described which matches overdrive suppression during the control period to that during drug action in order to cancel out the influence of changes in heart rate on ventricular automaticity.