Pitfalls of muscle palpation in TMJ diagnosis.
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Three sibs are described suffering from hereditary non-progressive spinal muscular atrophy with non-progressive mental retardation. One of them had in addition signs of pyramidal tract involvement. Muscular weakness was more pronounced proximally than distally and the neck muscles were severely involved. Th.ey all had small skulls and several associated congenital malformations were observed including syndactyly of the left hand in 1 patient. The patients belong to a small inbred community in the Netherlands. Erythropoietic protoporphyria was also present in the family but segregated independently. This combination of "congenital" mental retardation with "congenital" non-progressive spinal muscular atrophy is believed to represent a new syndrome, caused by a rare recessive gene.
Electromyograms, representing samples of neurological control signals, can be used to predict head rotation that can be either time optimal or non-time optimal, depending upon a given subject's intent. Kinematic factors such as operating levels in terms of horizontal and vertical position of the head from which horizontal rotations are made, importantly influence the tonic and phasic aspects of the EMG signal. Pairs of head-rotating muscles, splenius and sternocleidomastoideus muscles, demonstrate reciprocal innervation, particularly for time optimal head rotations. Head rotations of the same amplitude but different velocities correlate with pulse height and pulse width of envelopes of the rectified EMG. Rise of the agonistic EMG correlates in detail with rise of the acceleration transient for a given fast or slow head rotation. Our data demonstrate both the optimal control of details of head movements and the influence of the stretch reflex that strongly relates to initial head position and the velocity of the movements around the primary position. The results support the idea of higher level programmed control of head rotation in human subjects.
Fourteen patients were identified with (1) pain and sensory changes in a brachial plexus distribution, (2) aggravation of pain with use of the affected extremity, and (3) pain on palpation over the brachial plexus. All patients had minimal or no intrinsic hand muscle atrophy. Only one patient had cervical ribs. Nerve conduction studies were normal, and electromyography (EMG) showed mild chronic neuropathic changes in 2 patients. None of the patients responded to conservative therapy over a prolonged period (7-12 months). A compressive brachial plexopathy from abnormally attached or enlarged scalene muscles that affected both upper and lower trunks of the brachial plexus was found at surgery in all patients. In 13 patients, at least one fibrous band compressed the lower trunk of the brachial plexus. Therefore, neurogenic thoracic outlet syndrome can occur from cervical bands and scalene muscle anomalies without intrinsic hand muscle atrophy, cervical ribs, enlarged C7 transverse processes, or EMG abnormalities.
The case reported in this article demonstrates an unusual referral mechanism for signs and symptoms of the face and the oral cavity emanating from a traumatized trapezius muscle. A theory for this referral, based on central connections of nerves V, VII, IX, X, and XI, is proposed.
In anaesthetized and curarized rabbits, the cervical sympathetic nerve (CSN) stimulation induces in jaw elevator muscles a tension response which can be mimicked by the intravenous injection of adrenaline, noradrenaline and phenylephrine. This response, previously described and attributed to the contraction of muscle spindle fibres, is entirely mediated by alpha-adrenoceptors. The administration of phenoxybenzamine (2.5-3.5 mg/kg) markedly inhibits the responses to the sympathetic stimulation and to the injection of adrenergic agonists. Rauwolscine (1 mg/kg) reduces the development of tension induced by both CSN stimulation and noradrenaline injection without significantly affecting the response to phenylephrine. These data suggest the presence of postsynaptic alpha 1- and alpha 2-adrenoceptors in intrafusal muscle fibres. Moreover, the possibility that alpha 2-adrenoceptors may also have an extrasynaptic location is entertained.
In freely moving rats, mitral cells multiunit activity and vigilance states (EEG and neck muscles EMG) were recorded during stimulations by some odorous stimuli known from previous experiments to elicit distinct emotional behaviors. An awaking influence may be pointed out; the greatest awaking influence is noted for the opposite most biologically meaningful stimuli: odor of fox (predator of the rat) and odor of grouped rats. Mitral cells responsiveness is not only modulated by the biological meaning of the olfactory stimulus but is also under the control of the arousal level of the animal; it decreases from wakefulness (W) to slow wave sleep (SWS).
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Following extensive bilateral lateral hypothalamic damage, rats appear "somnolent." Cortical EEG shows persistent high voltage delta, reinforcing the impression of sleep. Preoperatively and postoperatively, we simultaneously measured cortical and subcortical (hippocampal and pontine) EEG, muscular events (neck muscle EMG and eye movement EOG), and behavior, which, as aggregates, differentially define quiet sleep, active sleep, and waking. Postoperatively, though cortical activity was persistently slow, subcortical EEG, muscular events, and behavior, as aggregates, revealed quiet sleep, active sleep, and waking, organized subcortically, intact and alternating, but disconnected from the persistent slow cortical activity. For example, preoperatively, active sleep included cortical low voltage fast activity, hippocampal theta, episodic pontine spike bursts, flat EMG, nd rapid eye movements, without any organized behavior. Postoperatively, the same aggregate of subcortical and muscular events indicated the presence of active sleep. Similarly so, for subcortically organized quiet sleep and spontaneous waking. Such waking, termed "drowsy-wakefulness," is a low-arousal form, perhaps related to drowsiness in other species, and to human hypersomnia.
EEG recording was performed, during nest-building behavior (NBB), from the hippocampus and sensorimotor cortex of nulliparous albino rats with simultaneous recordings of EMGs of neck-muscle and eye movements. The duration of NBB varied with a period of 4-5 days. However, the relative durations of behavioral transitions in NBB, i.e., nest-building, grooming, and sleeping, were regular in both long lasting and early terminated NBB. REM sleep was identified, in every instance, immediately after NBB. The latency of REM sleep was significantly tied to the termination of NBB without regard to the duration of NBB. Differences in the duration of NBB, however, affected REM-propensity: the longer the NBB was, the shorter the latency of REM sleep tended to be. NBB might accelerate the induction of the physiological condition responsible for REM sleep generation.
Acoustic startle responses were measured as part of a systematic attempt to determine if early protein malnutrition leads to a general hyperreactivity to aversive stimulation. In Experiment 1 startle responses transduced by floor movements were not reliably influenced by protein restriction in the preweaning or postweaning periods. The magnitude of the startle response, however, was positively correlated with body weight, partly as a consequence of the transduction method. Thus, differences in body weight might have obscured diet-related differences in startle amplitude. In Experiment 2 startles were recorded as electromyographic responses of the neck muscles and were larger in rats fed the low protein diet postweaning, especially in rats switched from high to low protein conditions at weaning. There was no indication that rats subjected to preweaning protein malnutrition were hyperreactive to aversive stimulation. In Experiment 1 it was also found that mean startle amplitudes were larger in young adults, 60 or 90 days old, than in 35-day-old rats, partly because there was less habituation in the adults.
In adult geese, chronic polygraphic recordings of EEG, EOG, EMG, ECG and respiratory rate completed with behavioral observations allowed the characterization of four states of vigilance: wakefulness (W), drowsiness (D), slow wave sleep (SWS) and paradoxical sleep (PS). The EEG, EOG, EMG general patterns observed during W, D, SWS and PS episodes with nuchal isotonia or hypotonia were similar to those reported in other birds. The characteristic brevity of avian PS was confirmed since this sleep state occupied only 2.8% of the nycthemere in geese. For the first time in an adult bird it was shown that numerous PS episodes were accompanied, as in mammals, by a total disappearance of nuchal EMG activity. These observations made in a bird species with a stable head support when sleeping, suggest that, as in mammals, inhibitory mechanisms leading to a PS related nuchal atonia do exist and that head falling is not the cause of PS episodes brevity in birds.
A previous study demonstrated that electrical stimulation of the amygdala facilitated the acoustic startle reflex. The purpose of the present study was to determine the temporal relationship between activation of the amygdala and its enhancement of the acoustic startle reflex. A single 0.1 msec pulse was delivered to the central nucleus of the amygdala at various times before or after the onset of 20 msec noise burst or a 0.1 msec click. Startle was enhanced when the stimulation occurred within 5 msec of the startle stimulus onset. Electromyographic recordings from the neck muscles demonstrated that the short 6 msec latency startle response was facilitated even when amygdala stimulation was presented 1.25 msec after the onset of the startle stimulus. This indicates that the time for the effects of amygdala stimulation to reach the brain stem startle circuit is less than 5 msec, suggesting a very direct pathway from the amygdala to the startle circuit. The similarity of this effect to fear-potentiated startle is also discussed.
We describe a system for the analysis of head displacement and angle. This system utilizes an inexpensive array of Hall effect transducers and associated electronics. Computer analysis of the output of the system permits real time display of head angle, position and associated velocity measures.
To determine whether spontaneous movement was associated with an organized respiratory response during early stages of mammalian development, we studied immature suckling opossums (Didelphis virginiana) between 30 and 60 days of age. Rate and depth of breathing were measured using pressure plethysmography and movement was assessed using electromyography of neck muscles. During air-breathing as well as during ventilatory chemostimulation with hypoxic, hypercapnic, and asphyxiant test gases, the onset of spontaneous movement was often marked by an increase in minute-ventilation, dominated by an increase in breathing frequency. In the absence of respiratory irregularities, ventilation and breathing frequency remained elevated throughout an episode of movement. After decerebration at the midcollicular level, the onset of spontaneous movement was accompanied by respiratory effects similar to those found in the intact preparation. The ventilation response with spontaneous movement contrasted to results during venilatory chemostimulation at rest, where increases in breathing resulted primarily from increases in tidal volume. It is concluded that a hyperpnea with spontaneous movement is present in the suckling opossum, and that the effect is primarily organized in the lower brainstem.
Ventilatory and waking responses to laryngeal stimulation were studied in six chronically tracheostomized lambs breathing through an endotracheal tube. A balloon catheter inserted in the rostral tracheal segment allowed application of distilled water onto the larynx. Apnea, the main primary ventilatory response, was shorter in wakefulness (7.9 sec) than in quiet (10.7 sec) or active sleep (10.6 sec, residual variance = 3.29), where the response to laryngeal stimulation was poorly reproducible. Arousal delay measured from the neck muscle EMG was longer in active (21.1 sec) than in quiet sleep (5.4 sec, residual variance = 9.05). Arousal preceded apnea termination more often in quiet than in active sleep. When breathing resumed a sigh frequently occurred following prolonged apneas. We conclude that laryngeal stimulation elicits apnea in all states in mature lambs. The termination of apnea is related to waking up in quiet but not in active sleep, where arousal is depressed. A comparison of our results with data from preterm and adult mammals strongly suggests that the ventilatory response to laryngeal stimulation during active sleep is unaffected by maturation.
The relative inspiratory augmentations of sternomastoid, scalene, external intercostal, interchondral and diaphragmatic electromyographic activities were examined during the progressive asphyxia induced by rebreathing in pentobarbitone/urethane anaesthetized rabbits. Diaphragmatic activity augmented significantly less than that of the scalene, intercostal and interchondral muscles in response to the asphyxic increase in inspiratory drive (hyperpnoea). Cervical vagotomy significantly increased the levels of inspiratory activity during the asphyxic hyperpnoea but did not abolish these relations. Dorsal rhizotomy at levels appropriate for the respective recording sites significantly limited the intercostal and interchondral augmentations, and depressed diaphragmatic activity to a less pronounced extent, but did not affect scalene activity. The asphyxic apnoea succeeding the hyperpnoea was terminated by gasping respiration. Excepting the interchondrals each muscle exhibited significantly greater electromyographic amplitudes during gasping than during the terminal hyperpnoeic efforts. Only during gasping were the sternomastoid muscles recruited. The intercostal and scalene gasps were significantly greater than those exhibited by either the interchondrals or the diaphragm. Such disproportionate responses were not affected by vagotomy or dorsal rhizotomy. The disparate inspiratory contributions during progressive asphyxia can therefore only be partially accounted for by differences in proprioceptive control.