Epileptiform electroencephalographic patterns

Electroencephalography (EEG) is the most useful test for assessment of patients with epilepsy. It can help establish the diagnosis of epilepsy and determine the type of seizure disorder and its site of origin. Epileptiform abnormalities in the EEG tracing may be focal or generalized. The main types of focal epileptiform discharges arise from the temporal, frontal, occipital, centroparietal, centrotemporal, and midline regions of the brain. Generalized epileptiform discharges consist of the 3-Hz spike-and-wave, slow spike-and-wave, atypical spike-and-wave, paroxysmal fast activity, and hypsarrhythmic patterns. Status epilepticus is manifested by continuous epileptiform discharges or recurrent seizure activity without interim recovery, which can occur in a generalized or focal manner. Benign epileptiform variants unassociated with seizures can also be present in the EEG. Included in this category are the "14 & 6" positive bursts, small sharp spikes, wicket waves, 6-Hz spike-and-wave discharges, and rhythmic temporal theta activity. The EEG findings should be interpreted in the context of the overall clinical picture.     

Fictive gill and lung ventilation in the pre- and postmetamorphic tadpole brain stem

The pattern of efferent neural activity recorded from the isolated brain stem preparation of the tadpole Rana catesbeiana was examined to characterize fictive gill and lung ventilations during ontogeny. In vitro recordings from cranial nerve (CN) roots V, VII, and X and spinal nerve (SN) root II of premetamorphic tadpoles showed a coordinated sequence of rhythmic bursts occurring in one of two patterns, pattern1, high-frequency, low-amplitude bursts lacking corresponding activity in SN II and pattern 2, low-frequency, high-amplitude bursts with coincident bursts in SN II. These two patterns corresponded to gill and lung ventilatory burst patterns, respectively, recorded from nerve roots of decerebrate, spontaneously breathing tadpoles. Similar patterns were observed in brain stem preparations from postmetamorphic tadpoles except that they showed a greater frequency of lung bursts and they expressed fictive gill ventilation in SN II. The laryngeal branch of the vagus (Xl) displayed efferent bursts in phase with gill and lung activity, suggesting fictive glottal constriction during gill ventilation and glottal dilation during lung ventilation. The fictive gill ventilatory cycle of pre- and postmetamorphic tadpoles was characterized by a rostral to caudal sequence of CN bursts. The fictive lung ventilatory pattern in the premetamorphic animal was initiated by augmenting CN VII discharge followed by synchronous bursts in CN V, X, SN II, and Xl. By contrast, postmetamorphic patterns of fictive lung ventilation were characterized by lung burst activity in SN II that preceded burst onset in CN V and followed the lead burst in CN VII. We conclude that recruitment and timing of pattern 1 and pattern 2 rhythmic bursts recorded in vitro closely resemble that recorded during spontaneous respiratory behavior, indicating that the two patterns are the neural equivalent of gill and lung ventilation, respectively. Further, fictive gill and lung ventilatory patterns in postmetamorphic tadpoles differ in burst onset latency from premetamorphic tadpole patterns and resemble fictive oropharyngeal and pulmonary burst cycles in adult frogs.     

The characteristics of the spontaneous activity of single neurons in the human ventrolateral thalamus during changes in the functional state of the brain

In the thalamic ventro-lateral nucleus of parkinsonian patients, two main types of convergent cells were shown to exist: 1) units with irregular discharges (A-cells, 74%) and 2) units with bursts of unstable rhythmic discharges (B-cells, 26%). The functional brain changes were accompanied by modifications of A-cells activity into the transient rhythmic burst-like pattern, characterized by two different types of intrinsic structure burst discharges being in some cases similar to the structure of B-cells. A correlation between activities of these units and the type of parkinsonian pathology was revealed.     

Origin of the synchronized network activity in the rabbit developing hippocampus

Rhythmic spontaneous bursting is a fundamental hallmark of the immature hippocampal activity recorded in vitro. These bursts or giant depolarizing potentials (GDPs) are GABA- and glutamatergic-driven events. The mechanisms of GDPs generation are still controversial, since although a hilar origin has been suggested, GDPs were also recorded from isolated CA3 area. Here, we have investigated the origin of GDPs in hippocampal slices from newborn rabbits. Simultaneous intracellular recordings were performed in CA3, CA1 and the fascia dentata. We found a high degree of correlation between the spontaneous GDPs present in CA3 and CA1 regions. Cross-correlation analysis demonstrated that CA3 firing precedes CA1 by about 192 ms, although a significant population of discharges was recorded first in CA1 (20%). Granule cells (GCs) in the fascia dentata also showed GDPs. The frequency of these events (1.46 +/- 1.25 GDPs/min, n = 7) is significantly lower when compared with that from CA3 (3.13 +/- 1.43 GDPs/min, n = 10) or CA1 (2.94 +/- 1.36 GDPs/min, n = 17). Dual recordings from CA3 and fascia dentata cells showed synchronous bursts in both regions with no prevalent preceding area. By recording from isolated areas we found that CA1, CA3 and the fascia dentata can produce GDPs, suggesting that they emerge as a property of local circuits present throughout the hippocampus.     

3-dimensional MR coronary angiography with navigator technique: imaging of the proximal course of a coronary artery anomaly

Severe congestive heart failure (CHF) is associated with Cheyne-Stokes (C-S) respiration, which may be an index of poorer prognosis. The mechanisms linking C-S respiration to poorer functional status and prognosis in patients with CHF are unknown. We tested the hypothesis that C-S respiration increases muscle sympathetic nerve activity (MSNA) in 9 patients with CHF. Oxygen saturation was 96 +/- 1% during normal breathing and 91 +/- 1% after the apneic episodes (p < 0.05). Mean blood pressure was 79 +/- 8 mm Hg during normal breathing and 85 +/- 8 mm Hg during C-S respiration (p = 0.001). C-S respiration increased MSNA burst frequency (from 45 +/- 5 bursts/min during normal breathing to 50 +/- 5 bursts/min during C-S respiration; p < 0.05) and total integrated nerve activity (to 117 +/- 7%; p < 0.05). We also studied an additional 5 patients in whom C-S breathing was constant, without any periods of spontaneous normal breathing. In these patients, MSNA was higher (65 +/- 5 bursts/min) than MSNA in patients in whom C-S breathing was only intermittent (45 +/- 5 bursts/min; p < 0.05). In all 14 patients, the effects of different phases of C-S respiration were examined. MSNA was highest during the second half of each apnea (increasing to 152 +/- 14%; p < 0.01) and blood pressure was highest during mild hyperventilation occurring after termination of apnea (p < 0.0001). We conclude that C-S respiration decreases oxygen saturation, increases MSNA, and induces transient elevations in blood pressure in patients with CHF.     

GABA-receptor-independent dorsal root afferents depolarization in the neonatal rat spinal cord

Dorsal root afferent depolarization and antidromic firing were studied in isolated spinal cords of neonatal rats. Spontaneous firing accompanied by occasional bursts could be recorded from most dorsal roots in the majority of the cords. The afferent bursts were enhanced after elevation of the extracellular potassium concentration ([K+]e) by 1-2 mM. More substantial afferent bursts were produced when the cords were isolated with intact brain stems. Rhythmic afferent bursts could be recorded from dorsal roots in some of the cords during motor rhythm induced by bath-applied serotonin and N-methyl--aspartate (NMDA). Bilaterally synchronous afferent bursts were produced in pairs of dorsal roots after replacing the NaCl in the perfusate with sodium-2-hydroxyethansulfonate or after application of the gamma-aminobutyric acid-A (GABAA) receptor antagonist bicuculline with or without serotonin (5-HT) and NMDA. Antidromic afferent bursts also could be elicited under these conditions by stimulation of adjacent dorsal roots, ventrolateral funiculus axons, or ventral white commissural (VWC) fibers. The antidromic bursts were superimposed on prolonged dorsal root potentials (DRPs) and accompanied by a prolonged increase in intraspinal afferent excitability. Surgical manipulations of the cord revealed that afferent firing in the presence of bicuculline persisted in the hemicords after hemisection and still was observed after removal of their ventral horns. Cutting the VWC throughout its length did not perturb the bilateral synchronicity of the discharge. These findings suggest that the activity of dorsal horn neurons is sufficient to produce the discharge and that the bilateral synchronicity can be maintained by cross connectivity that is relayed from side to side dorsal to the VWC. Antagonists of GABAB, 5-HT2/5-HT1C, or glutamate metabotropic group II and III receptors could not abolish afferent depolarization in the presence of bicuculline. Depolarization comparable in amplitude to DRPs, could be produced in tetrodotoxin-treated cords by elevation of [K+]e to the levels reported to develop in the neonatal rat spinal cord in response to dorsal root stimulation. A mechanism involving potassium transients produced by neuronal activity therefore is suggested to be the major cause of the GABA-independent afferent depolarization reported in our study. Possible implications of potassium transients in the developing and the adult mammalian spinal cord are discussed.     

Requirement of protein synthesis for group I mGluR-mediated induction of epileptiform discharges

Picrotoxin (50 microM) elicited rhythmic synchronized bursting in CA3 pyramidal cells in guinea pig hippocampal slices. Addition of the selective group I metabotropic glutamate receptor (mGluR) agonist (S)-3,5-dihydroxyphenylglycine (25 microM) elicited an increase in burst frequency. This was soon followed by a slowly progressive increase in burst duration (BD), converting the brief 250-520 ms picrotoxin-induced synchronized bursts into prolonged discharges of 1-5 s in duration. BD was significantly increased within 60 min and reached a maximum after 2-2.5 h of agonist exposure. The protein synthesis inhibitors anisomycin (15 microM) or cycloheximide (25 microM) significantly impeded the mGluR-mediated development of the prolonged bursts; 90-120 min of agonist application failed to elicit the expected burst prolongation. By contrast, the mGluR-mediated enhancement of burst frequency progressed unimpeded. Furthermore, protein synthesis inhibitors had no significant effect on the frequency or duration of fully developed mGluR-induced prolonged discharges. These results suggest that the group I mGluR-mediated prolongation of synchronized bursts has a protein synthesis-dependent mechanism.     

Breastfeeding experience and breast cancer risk among postmenopausal women

A method of automated detection of onset and termination of rhythmic muscle activity in electromyograms (EMGs) is presented. A threshold level in the EMG is computed, such that amplitudes in the EMG signal exceeding this level indicate muscle activity. The threshold level is determined using a statistical criterion based on the amplitude distribution of the entire EMG signal. The working of the method is illustrated with EMG signals recorded from chewing muscles. EMG signals with a good as well as a worse signal-to-noise ratio are presented. The method can be used for any EMG signal containing cyclic bursts of activity and thus may be applied in studies on rhythmic movements, such as chewing, walking and breathing. An automated method of EMG burst detection has the advantage that large amounts of EMG data can be easily and objectively processed.     

The use of system identification techniques in the analysis of oculomotor burst neuron spike train dynamics

The objective of system identification methods is to construct a mathematical model of a dynamical system in order to describe adequately the input-output relationship observed in that system. Over the past several decades, mathematical models have been employed frequently in the oculomotor field, and their use has contributed greatly to our understanding of how information flows through the implicated brain regions. However, the existing analyses of oculomotor neural discharges have not taken advantage of the power of optimization algorithms that have been developed for system identification purposes. In this article, we employ these techniques to specifically investigate the "burst generator" in the brainstem that drives saccadic eye movements. The discharge characteristics of a specific class of neurons, inhibitory burst neurons (IBNs) that project monosynaptically to ocular motoneurons, are examined. The discharges of IBNs are analyzed using different linear and nonlinear equations that express a neuron's firing frequency and history (i.e., the derivative of frequency), in terms of quantities that describe a saccade trajectory, such as eye position, velocity, and acceleration. The variance accounted for by each equation can be compared to choose the optimal model. The methods we present allow optimization across multiple saccade trajectories simultaneously. We are able to investigate objectively how well a specific equation predicts a neuron's discharge pattern as well as whether increasing the complexity of a model is justifiable. In addition, we demonstrate that these techniques can be used both to provide an objective estimate of a neuron's dynamic latency and to test whether a neuron's initial firing rate (expressed as an initial condition) is a function of a quantity describing a saccade trajectory (such as initial eye position).     

Central generation of grooming motor patterns and interlimb coordination in locusts

Coordinated bursts of leg motoneuron activity were evoked in locusts with deefferented legs by tactile stimulation of sites that evoke grooming behavior. This suggests that insect thoracic ganglia contain central pattern generators for directed leg movements. Motoneuron recordings were made from metathoracic and mesothoracic nerves, after eliminating all leg motor innervation, as well as all input from the brain, subesophageal ganglion, and prothoracic ganglion. Strong, brief trochanteral levator motoneuron bursts occurred, together with silence of the slow and fast trochanteral depressor motoneurons and activation of the common inhibitor motoneuron. The metathoracic slow tibial extensor motoneuron was active in a pattern distinct from its activity during walking or during rhythms evoked by the muscarinic agonist pilocarpine. Preparations in which the metathoracic ganglion was isolated from all other ganglia could still produce fictive motor patterns in response to tactile stimulation of metathoracic locations. Bursts of trochanteral levator and depressor motoneurons were clearly coordinated between the left and right metathoracic hemiganglia and also between the mesothoracic and the ipsilateral metathoracic ganglia. These data provide clear evidence for centrally generated interlimb coordination in an insect.     

Ectopic impulse generation and autoexcitation in single myelinated afferent fibers in patients with peripheral neuropathy and positive sensory symptoms

Microneurographic studies were performed using cutaneous nerves of 8 patients with documented peripheral neuropathy who expressed positive sensory symptoms. Intraneural recordings in single myelinated fibers revealed: (i) ectopic generation of bursts of spontaneous action potentials; (ii) ectopic generation of ongoing repetitive discharges transiently interrupted by natural stimulation of the receptive field; and (iii) repetitive discharges triggered by a preceding action potential. These results provide direct evidence of a peripheral pathophysiological basis for spontaneous and stimulus-induced paresthesias and dysesthesias in patients with peripheral neuropathy.     

Mixed IgM kappa-IgM lambda cryoglobulinemia with a double monoclonal serum component. A case report

The regulation of breathing is dependent on the complex interaction of three components of the respiratory system: 1) the control centers, 2) the sensors, and 3) the effector organs. The control centers reside in the brainstem and are responsible for the automaticity of breathing. Input into these respiratory centers can be initiated from higher brain centers in order to produce voluntary breathing efforts. Afferent neural signals also come to the central control system from the respiratory sensors, which are divided into two categories: chemoreceptors and sensory receptors. The chemoreceptors respond to changes in the blood oxygen, carbon dioxide, and hydrogen ion concentration by sending impulses to the control center to alter the ventilatory pattern by affecting the effector organs--the respiratory muscles. The sensory receptors are located in the upper and lower airways, the lung, and the muscles of respiration. They also can have a marked effect on the respiratory pattern. It is believed that stimulation of these receptors is important in the initiation of hyperventilation and cough in lung diseases such as asthma. There is also recent evidence that respiratory chemoreceptor responsiveness is abnormal in patients with asthma who have a history of near-fatal attacks.     

Effects of conditioned aversive stimuli presented during tonic immobility in guinea pigs.

The duration of and susceptibility to tonic immobility were measured in 3 groups of albino and pigmented guinea pigs (N = 27) while a train of intense tone bursts was presented. In 1 group, the tone bursts had been previously associated with painful shock stimuli. The 2nd group had previously experienced the tone bursts alone, and the 3rd group had previously received shocks without the train of tone bursts. Results indicate that both groups which had previously received shock exhibited increased susceptibility to immobilization, and the no-shock group showed a decline in duration when tone bursts were presented. Results could not be easily interpreted to support the fear hypothesis. Explanations involving "sensitization" and "learned helplessness" are proposed. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Auditory continuity and loudness computation

Sequences composed of alternating bursts of different levels with no silences separating them can give rise to a perception of a continuous sound upon which is superimposed an intermittent stream. These experiments sought to determine how the perceived loudness of the intermittent stream depends on the level difference between higher-level and lower-level bursts in the sequence in cases in which continuity is either heard or not heard. In the main experiment, listeners were asked to adjust the level of continuous or intermittent comparison sequences to match the loudness of components that appeared to be either continuous or intermittent in an alternating-level reference sequence, thus urging them to focus on the two-stream percept. Loudness matches of continuous comparison stimulus were close to physical levels of the lower-level bursts, whereas matches of the intermittent comparison stimulus were well below the physical levels of higher-level bursts. These results are discussed in terms of Bregman's [Auditory Scene Analysis (MIT, Cambridge, MA, 1990)] "old-plus-new" hypothesis: The loudness of the intermittent stream should result from the subtraction of the lower level from the higher level under the assumption that the higher-level burst represents a simultaneous mixture of sounds including the continuation of the lower-level burst. Additional experiments verified that, in the absence of the continuity phenomenon, matched levels were very close to the physical levels and that matches to fixed-level continuous and intermittent sequences were precise. The matching results from the main experiment support predictions of neither classical loudness models that do not take auditory organization processes into account nor schema-based models that presume a selection of information from the higher-level burst that does not affect the perceptual content of this burst. The matched levels fell between predictions of models based on subtraction of acoustic pressure and acoustic power, but were very different from subtraction of loudness measured in sones, suggesting that loudness is computed subsequent to auditory organization processes.     

Development of localized oriented receptive fields by learning a translation-invariant code for natural images

In this study we present a computer model of a pacemaker cell subjected to vagal stimulation. This model allows us to investigate the entrainment phenomena of the pacemaker cell resulting from its dynamic interaction with a periodic train of vagal bursts. The possibility of entrainment depends mainly on the fact that a vagal stimulation discharge can "correct" the pacemaker rhythm by an amount that depends on its instantaneous relationship to the pacemaker cycle length. This very simple model, is based on the two most important functional properties of the cardiac pacemaker cells. The first property is the intrinsic pacemaker cycle length, which is an "internal" parameter of the cell, describing the most basic feature of a pacemaker cell. The second one is the phase response curve (PRC), which is an "overall collective" function, containing all the "information" about the possible interactions between the pacemaker cell and the outside world (i.e. its interaction with surrounding cells, external stimulus, etc.). A "collective" PRC was reconstructed from the resulting effects of all the pulses composing a burst. It appears that the PRC parameters as well as the vagal burst parameters are important factors in predicting the entrainment phenomena. Specifically, we found that the tendency of the pacemaker cell to become synchronized with bursts of vagal activity is greater, the larger the number of pulses per burst. However, increasing the number of pulses may also increase the tendency of the pacemaker towards instability, which was unveiled as changes in the configuration of the "collective" PRC. We applied the periodic train of vagal bursts so as to simulate the respiratory sinus arrhythmia (RSA) modulation on the pacemaker cell. We included also a modulation of sympathetic origin, represented as periodic changes in the intrinsic pacemaker cycle length. The frequency response of the pacemaker to "autonomic" modulations allowed us to demonstrate that the RSA dynamics can be interpreted in terms of the entrainment of the pacemaker cell by the respiratory modulation of vagal activity.     

Angiitis of the central nervous system in systemic diseases

PURPOSE: This review is aimed at presenting classification and diagnosis criteria of isolated central nervous system (CNS) angiitis, and at proposing guidelines for diagnosis and management of this disease. CURRENT KNOWLEDGE AND KEY POINTS: Isolated CNS angiitis are rare and most information has been provided by studies of very small series. Angiitis can be primitive or secondary to infectious, neoplastic diseases, or toxics. Clinical manifestations and radiologic abnormalities are not specific. A brain biopsy is therefore often required to confirm the diagnosis, as numerous non-inflammatory vascular diseases can mimic both clinically and radiologically isolated CNS angiitis. PERSPECTIVES AND PROJECTS: To help guide the diagnosis and therapeutical management of patients with CNS angiitis, strict classification criteria should be used: 1) rule out the various diseases that can mimic clinical and radiological CNS aspects related to isolated angiitis and differentiate "isolated CNS angiitis" from "CNS angiitis associated with systemic diseases"; 2) search for factors associated with the development of a "secondary CNS angiitis"; 3) check presumed mechanism at the origin of the cerebral vascular disease: "angiitis" versus "angiopathy"; 4) if the diagnosis of "primary CNS angiitis" is still suspected, it seems reasonable to perform cerebral and leptomeningeal biopsies. Treatment is still unknown and has to be discussed on a case by case basis according to the severity and progression of symptoms.     

Mechanism of the human diving response

The diving response in human beings is characterized by breath-holding, slowing of the heart rate (diving bradycardia), reduction of limb blood flow and a gradual rise in the mean arterial blood pressure. The bradycardia results from increased parasympathetic stimulus to the cardiac pacemaker. The reduction in limb blood flow is due to vasoconstriction resulting from increased activity of the sympathetic nerves supplying arteries in the arms and legs. Essentially the response is produced by the combination of water touching the face and either voluntary or involuntary (reflex) arrest of breathing. The nervous inputs and outputs for the response are coordinated in the brain stem by the respiratory, vasomotor and cardioinhibitory "centers." The diving response in human beings can be modified by many factors but the most important are water temperature, oxygen tension in the arterial blood and emotional factors.     

Nociceptive integration in the rat spinal cord: role of non-linear membrane properties of deep dorsal horn neurons

Deep dorsal horn neurons (DHNs) involved in nociception can relay long-lasting inputs and generate prolonged afterdischarges believed to enhance the transfer of nociceptive responses to the brain. We addressed the role of neuronal membrane properties in shaping these responses, by recording lamina V DHNs in a slice preparation of the rat cervical spinal cord. Of 256 neurons, 102 produced accelerating discharges in response to depolarizing current pulses, whereas the other neurons showed spike frequency adaptation. Two mechanisms mediated the firing acceleration: a slow inactivation of a K+ current expressed upon activation of the neuron from hyperpolarized holding potentials, and the expression of a regenerative plateau potential activating around resting membrane potential. The increase in firing frequency was much stronger when sustained by the plateau potential (71 DHNs, 28%). A few neurons produced adaptation and both types of acceleration, in different membrane potential domains, showing that the firing pattern of a deep DHN is not a rigid characteristic. Plateau potentials could be elicited by stimulation of nociceptive primary afferent fibres. The bistability associated with plateau potentials permitted afterdischarges. Because plateau potentials had slow activation kinetics and were voltage-dependent, the neurons had non-linear input-output relationships in both the amplitude and time domains. Nociceptive primary afferent stimulation elicited intense and prolonged responses in plateau-generating DHNs, while brief bursts of spikes were evoked otherwise. These results indicate that in a population of deep DHNs, intense firing and prolonged afterdischarges in response to nociceptive stimulation depend on non-linear intrinsic membrane properties.     

Features of ipsilaterally evoked inhibition in the dorsal nucleus of the lateral lemniscus

The dorsal nucleus of the lateral lemniscus (DNLL) is a binaural nucleus whose neurons are excited by stimulation of the contralateral ear and inhibited by stimulation of the ipsilateral ear. Here we report on several features of the ipsilaterally evoked inhibition in 95 DNLL neurons of the mustache bat. These features include its dependence on intensity, its tuning and the types of stimuli that are capable of evoking it. Inhibition was studied by evoking discharges with the iontophoretic application of glutamate, and then evaluating the strength and duration of the inhibition of the glutamate evoked background activity produced by stimulation of the ipsilateral ear. Excitatory responses were evoked by stimulation of the contralateral ear with best frequency (BF) tone bursts. Glutamate evoked discharges could be inhibited in all DNLL neurons and the inhibition often persisted for periods ranging from 10 to 50 ms beyond the duration of the tone burst that evoked it. The duration of the persistent inhibition increased with stimulus intensity. Stimulus duration had little influence on the duration of the persistent inhibition. Signals as short as 2 ms suppressed discharges for as long as 30 ms after the signal had ended. The frequency tuning of the total period of inhibition and the period of persistent inhibition were both closely matched to the tuning evoked by stimulation of the contralateral ear. Moreover, the effectiveness of complex signals for evoking persistent inhibition, such as brief FM sweeps and sinusoidally amplitude and frequency modulated signals, was comparable to that of tone bursts at the neuron's excitatory BF, so long as the complex signal contained frequencies at or around the neuron's excitatory BF. We also challenged DNLL cells with binaural paradigms. In one experiment, we presented a relatively long (40 ms) BF tone burst of fixed intensity to the contralateral ear, which evoked a sustained discharge, and a shorter, 10 ms signal of variable intensity to the ipsilateral ear. As the intensity of the 10 ms ipsilateral signal increased, it generated progressively longer periods of persistent inhibition and thus the discharges were suppressed for periods far longer than the 10 ms duration of the ipsilateral signal. With interaural time disparities, ipsilateral signals that led contralateral signals evoked a persistent inhibition that suppressed the responses to the trailing contralateral signals for periods of a least 15 ms. This suggests that an initial binaural sound that favors the ipsilateral ear should suppress the responses to trailing sounds that normally would be excitatory if they were presented alone. We hypothesize a circuit that generates the persistent inhibition and discuss how the results with binaural signals support that hypothesis.     

Control of respiration in newborn babies. IV. Rib cage stability and respiratory regulation

The recordings from an earlier study regarding the respiratory depth and rate changes induced by exposure to 4% CO2 in air in 13 babies with PM age varying between 32 and 43 weeks were reexamined with regard to the pattern of thoracic abdominal breathing excursion in breathing immediately prior to the CO2 exposure and the type of response induced. The pattern was called "stable" when the thoracic breathing excursions were in phase and congruent with the abdominal ones. When the thoracic excursions in comparison with the abdominal excursions were totally inverted, or incongruous but in phase, or rapidly varying between those two, the pattern was called "unstable". "Unstable" pattern of the breathing prior to the CO2 exposures was followed in an incidence of 60% by the type of response to CO2 which is characterized by a prompt rate increase (the "Type B" response) and only in 16% by the type characterized by an increased breathing amplitude (the "Type A" response). When the excursion pattern of the breathing prior to the CO2 exposures was "stable" "Type A" responses were induced in 59% and "Type B" responses in only 14%. The excursion pattern present when a baby is exposed to 4% CO2 thus seems to affect the type of respiratory depth and rate changes achieved. With increasing postmenstrual age the excursion pattern of the spontaneous breathing is more often "stable" and respiratory depth and rate changes of the "Type B" induced by CO2 less common. The variabilities of the breathing seen preferably in the preterm baby regarding regularity, rate and tidal volumes (as they could be approximated by the registration methods used) were noted most when the excursion pattern was "unstable". The results can be hypothetically interpreted to indicate a dynamic interaction between the thoracic wall and pulmonary mechanoreceptor systems of respiratory regulation. The decreasing variability of the breathing seen with increasing maturation in the baby could be explained by an increasing maturation of the neuromuscular ability to provide stability to the rib cage which would act stabilizing on the pulmonary vagal afferent input to the respiratory center.