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By K. Sven. John Jay College of Criminal Justice.

B: The extracardiac Fontan uses a tube graft to connect the inferior vena cava to the central pulmonary artery buy zovirax 800 mg visa. In both cases all caval return with the exception of the coronary sinus is directed to the pulmonary arteries purchase 800 mg zovirax free shipping, simulating as closely as possible the normal circulatory pattern purchase zovirax 400 mg with visa. To improve hemodynamics, especially in the early postoperative period, a fenestration is often placed between the baffle or conduit and the pulmonary venous atrium. This decreases central venous pressure and increases preload to the single ventricle, albeit at the cost of some systemic desaturation. For patients who have undergone a stage 2 procedure, either a bidirectional Glenn shunt or hemi-Fontan, the timing of completion Fontan is not critical; in general, the operation is performed between 18 months and 4 years of age, with anesthetic considerations similar to those for the stage 2 operation. Although interventional techniques to perform the completion Fontan using coated stents have been reported, much more commonly this is performed in the operating room using one of two techniques; a lateral tunnel or extracardiac conduit (Fig. As part of the hemi-Fontan, a dam is constructed between the pulmonary arteries and the right atrium. During the completion Fontan, this dam is removed and a section of prosthetic conduit is used to create a baffle to route the inferior caval blood return to the pulmonary artery. Additional advantages include a low level of power loss as determined by computational fluid dynamic studies (369). Although controversial, some studies suggest a higher incidence of sinus node dysfunction following the lateral tunnel Fontan (370,371,372,373,374). Another potential disadvantage of the lateral tunnel Fontan involves the presence of prosthetic material exposed to the pulmonary venous portion of the atrium with the potential for thrombus formation and systemic embolization. The advantages include the ease of the operation and, although somewhat controversial, probably a lower incidence of sinus node dysfunction (370,371,372,373,374). In addition, no prosthetic material is placed in the pulmonary venous atrium, with potentially lower risk of thromboembolic complications. To this end, larger conduits, between 20 and 22 mm in diameter, are placed to accommodate growth. The larger and longer conduits may result in power loss, which, when combined with the potential for late revision for outgrowth, may impact the durability of the extracardiac Fontan. The use of a fenestration has resulted in excellent survival and shorter hospital stay (238). Additional strategies that minimize postoperative hospital stay include routine use of the diuretics including spironolactone, an aldosterone antagonist, and furosemide. Supplemental oxygen is used as a pulmonary vasodilator, and afterload reduction is given to improve cardiac output and lower single-ventricle filling pressures (375). Outcomes for Staged Palliation Most mortality associated with the staged surgical approach occurs during and after stage 1 palliation, with recent cumulative early and interstage mortality in the 5% to 30% range (88,273,376,377). Improved outcome has been associated with early diagnosis, preoperative stabilization, early repair, systematic management approaches, and increased monitoring both in-hospital and at home (86,88,345). Patient-related characteristics are increasingly recognized as risk factors for early and intermediate mortality after stage 1 palliation. Few studies have reported worsened outcomes in patients with prematurity, low birth weight, extracardiac anomalies, genetic syndromes, and/or additional cardiac anomalies. Patients with any of these characteristics have been designated as “high-risk” for staged palliation due to early operative mortality rates of 30% to 50% compared to 10% to 15% operative mortality in patients without the any of the aforementioned characteristics, the “standard-risk” cohort (90,378). We recently reported that intensive perioperative monitoring, early goal-directed treatment of shock and greater resource utilization offset the vulnerability of “high-risk” patients resulting in comparable operative survival in “high-risk” and “standard-risk” patients, 87% versus 95%, respectively. In this series, ability to achieve stage 2 palliation or progression to transplant in lieu of stage 2 palliation was comparable between risk groups. Overall, for this cohort of 162 consecutive patients, operative survival was 91%, 1-year survival was 90%, and survival at last follow-up was 86%. Although cardiac catheterization has been commonly preformed prior to stages 2 and 3 it may be indicated during the neonatal period or as part of post-Fontan management. One-year survival and survival to date are lower in high-risk patients compared to standard-risk patients (p = 0. Perioperative monitoring in high-risk infants after stage 1 palliation of univentricular congenital heart disease. This was performed in a group of patients that were listed for cardiac transplantation. Cardiac catheterization after stage 1 palliation and prior to stage 2 palliation may be indicated for shunt stenosis, atrial septal defect enlargement or recurrent arch obstruction. Information obtained at catheterization would include the measurement of pulmonary artery pressure, pulmonary capillary wedge pressure, right ventricular systolic and diastolic pressures, and pressures in the ascending and descending aorta. The operators should be prepared to perform interventions as needed on the pulmonary arteries, atrial septum, and arch. In selected patients in whom clinical or anatomic concerns are absent by history, physical examination, and echocardiography, cardiac catheterization may not be necessary prior to stage 2 palliation (381). Indications may include excessive cyanosis that may be due to venovenous collateral or stenotic cavopulmonary connections or branch pulmonary artery stenoses. Catheter intervention for aortic arch narrowing occasionally may also be necessary after stage 2 palliation (249,360). Catheterization is routinely performed prior to the completion Fontan operation in many institutions. Important measurements to determine suitability of Fontan palliation include; pulmonary artery pressure, pulmonary capillary wedge pressure, and ventricular end-diastolic pressure. Cardiac catheterization following the Fontan operation may be necessary if there are anatomic or physiologic concerns not easily elucidated by noninvasive imaging techniques. Some centers routinely perform cardiac catheterization 6 to 12 months after the Fontan procedure with consideration for fenestration closure following hemodynamic assessment. In a report of five patients who underwent the Fontan operation with this technique, all returned home in 24 hours, however several patients required subsequent intervention for baffle leak (245). Late Fontan Concerns Staged palliation for single-ventricle physiology has undergone a series of surgical revisions that have reduced early postoperative Fontan mortality from 20% to less than 2% (391,392). Despite the significant morbidities associated with the Fontan operation, overall late mortality (range 4 months to 18 years) continues to decrease from 25% in the early experience to 5% in the recent era (392,393). Indications for successful Fontan have been modified from the initial “Ten Commandments” described by Choussat and Fontan. This list does specify physiologic risk factors for a failing Fontan that prevail and relate to ventricular performance, atrioventricular and aortic valve function, and pulmonary circulation (395). In addition, more complex anatomy that requires main pulmonary artery to ascending aorta anastomoses or ventricular septal defect enlargement, both indicators of ventricular outflow obstruction, has been identified as a risk factor for late morbidity. Ventricular Dysfunction Volume unloading provided by staged palliation results in reduction in ventricular size and wall thickness that, in turn, increases contractility and ventricular performance. Regardless of the early success with staged palliation, late ventricular dysfunction after the Fontan operation may ensue due to morphologic/structural features of the single right systemic ventricle, residual obstructive lesions, and/or atrioventricular valve insufficiency. The failing systemic ventricle after staged palliation can be attributed to systolic dysfunction, diastolic dysfunction, or both (396,398,399,400). Systolic dysfunction is characterized by reduced contractility and an ejection fraction of less than 50%. Diastolic dysfunction is more difficult to define, but is evident by increased ventricular end-diastolic pressure and the rate of ventricular relaxation (401,402). As a result, late ventricular dysfunction and subsequent failure of Fontan circulation become clinically evident with symptoms of lower functional class, exercise intolerance, dyspnea, fatigue, and syncope (403,404).

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This rapid regulation of flow by neural mechanisms is effected through reflex circuits best order for zovirax, composed of an afferent limb cheap zovirax 400mg line, which transmits information about the physiologic state to an integrating site within the medulla oblongata buy generic zovirax line, which, by modulating activity within the efferent limb of the autonomic nervous system mediates changes in vascular tone. The most powerful afferent limb of neural control originates within mechanoreceptors in the carotid sinuses and aortic arch, which respond to changes in arterial pressure (baroreceptors). At least two types of baroreceptors have been identified, with the first controlling dynamic changes in blood pressure and the second being responsible for control of resting blood pressure (14). Alterations in tension within these receptors modulate nerve impulses to the cardioregulatory and vasomotor centers of the medulla oblongata, which regulate the output in the efferent limb of the reflex (below). As a result, an increase in arterial pressure by stimulating the carotid sinus results in slowing of the heart rate, vasodilation, and a restoration of arterial pressure. These baroreceptors themselves are innervated by efferent fibers of the sympathetic nervous system, which suggests that sympathetic activity may modify the “gain” of the baroreceptor responses. Given the profound influence of the carotid sinus baroreceptors on arterial pressure, there is increasing interest in the potential for chronic carotid sinus stimulation to treat resistant systemic hypertension (15). They are located in the walls of both atria at the venoatrial junctions (16), and are scattered throughout the left ventricle and interventricular septum. Type A receptors fire during atrial contraction and respond to changes in atrial pressure, and type B receptors fire during ventricular systole and respond to changes in atrial volume (17). In particular, atrial receptors modulate the sympathetic activity to the renal vasculature (14), which combined with their influences on hormonal function (below) mediates their profound influence on intravascular volume. The first fire in a pulsatile manner in time with cardiac rhythm and are small in number. The second respond to mechanical stimulation and to various drugs and chemicals through nonmyelinated afferent nerves known as C fibers. Stimulation of C fibers, which are primarily located in the left ventricle results in hypotension and bradycardia through parasympathetic stimulation and sympathetic inhibition (16). Significant additional afferent inputs into the neural control of the circulation come from chemoreceptors, which are primarily located in the carotid body, aortic arch, and brain, as well as in coronary vessels, muscle, and lung. It appears that under normoxemic and normocapneic conditions, they exert little effect, but they are important in modulating the cardiorespiratory response to hypoxemia and hypercapnia. The most important central integrating site for these neural inputs for control of the circulation is in the medulla oblongata. The activity of these medullary centers may be modified by other centers within the brain, in particular, the hypothalamus. Central mechanisms in the medulla regulate the output of the sympathetic and parasympathetic neural systems, the efferent limb of neural control of the circulation. The primary efferent effectors are the sympathetic vasoconstrictor fibers, which when stimulated release norepinephrine from their nerve-endings. Other substances are also released, including monoamines, polypeptides, purines, and amino acids, some of which have direct vasoactive effects while others modulate the release, actions, and reuptake of norepinephrine (14). Impulses carried through vasoconstrictor fibers contribute to the normal vascular tone or baseline constriction that is present at rest in most vascular beds; thus they are the main mechanism for regulating blood pressure in the unstressed state. These vasoconstrictor fibers are prevalent in skeletal muscles, where intrinsic tone is fairly high under resting conditions. Sympathetically mediated venoconstriction modulates venous capacitance, and in turn, circulating volume. The transmitter in vasodilator fibers is thought to be acetylcholine, although in primates it may be epinephrine. These vasodilator fibers may cause a small anticipatory increase of blood flow to the skeletal muscle. However, once muscle exercise begins, local vasodilation probably plays a more important role (18). The parasympathetic system primarily controls heart function and rate although it does have a limited role in control of the peripheral circulation, through the release of acetylcholine. Parasympathetic vasodilator fibers are found in the cerebral and myocardial circulations and in the bladder, rectum, and external genitalia. These receptors are responsive to both locally produced catecholamines, originating from the local sympathetic innervation, endogenous circulating catecholamines from the adrenal, as well as to exogenous sympathomimetic drugs. Stimulation of the so-called α-adrenergic receptors results in vasoconstriction, while stimulation of β-adrenergic receptors causes vasodilation. The juxtaglomerular apparatus in the kidney secretes renin in response to decreased renal arterial pressure or a decrease in extracellular fluid volume. Another group of hormones that participate in regulation of the systemic circulation are the natriuretic peptides. Local Control by the Endothelium The vascular endothelium plays a key role in regulating vascular tone, by producing a variety of substances which mediate either relaxation (vasodilation) or contraction (vasoconstriction) of the underlying vascular smooth muscle (21). Several vasoconstrictor substances are also produced by the endothelium and again have been reviewed elsewhere. More recently, the role of the very potent mediator urotensin, which again can mediate both vasoconstriction and vasodilation, is receiving attention (22). Local Control by Metabolism Flow to many tissues of the body is regulated by changes in local metabolic demand. It appears that the “switch,” which couples increases in metabolism to local vasodilation resides in metabolism-related changes within the local chemical microenvironment. Many cells other than endothelial cells will release the potent vasodilator adenosine, in response to increased metabolism or decreased oxygen tension. Local Control by Red Blood Cells There is increasing interest in the regulation of local flow by red blood cells (23). Local Control by Autoregulation The ability for local flow to remain relatively constant over a range of arterial input pressures is particularly important for organs which cannot significantly alter their metabolic requirements in the face of hypotension. Potential mechanisms include an intrinsic myogenic response within the vascular smooth muscle, which allows the arterioles to constrict via an endothelial-independent mechanism in response to changes in transmural pressure. This possibly occurs through the interactions of cell surface integrins with extracellular matrix proteins and alterations in calcium currents (25). Alterations in the production of local metabolic factors, changes in sympathetic tone, and in the kidney, “tubular glomerular feedback” (below) are also likely to contribute. Flow to Specific Vascular Beds The dynamic interplay between the different mechanisms described above, mediate the variability in flow within and between the different regional vascular beds. As a general principle, the metabolically highly active organs such as the brain and heart are primarily regulated by local mechanisms, whereas the less active organs are more subject to central neural and hormonal controls. Specialized beds such as the renal and hepatic circulations, which receive blood for unique activities such as metabolic degradation and excretion, hematopoiesis, and blood pressure control, have unique combinations of control mechanisms. The myocardium is not discussed here, but is considered elsewhere in this textbook. The Cerebral Circulation The cerebral circulation has been the most extensively studied and characterized. First, there is a blood–brain barrier created by a continuous lining of endothelial cells linked by tight junctions, which provides some resistance to changes in concentrations of various circulating constituents such as H+ and catecholamines. Second, a significant component of the cerebral vascular resistance is formed by the large arteries, which appear to respond in a similar fashion to the arterioles in response to stresses such as hypoxia. Third, the cerebral circulation is encased in a closed box, the skull, so that tissue pressure is an important determinant of flow.

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The acceleration of the isovolumetric spike is measured from the baseline to the peak buy zovirax 200mg overnight delivery. The motion of the speckles in 2-D or even 3-D space can be used to calculate myocardial deformation discount zovirax 400 mg on-line. This image is taken from an apical two-chamber view 200 mg zovirax sale, and speckles within the inferior wall are magnified. The way these speckles move can be traced in 2-D on a frame-by-frame basis as illustrated in the right panels. The left upper panel represents the strain curves obtained from the apical three-chamber view, the left lower panel represents the strain curves obtained from the apical two-chamber view, and the right upper panel represents the strain curves from the apical four-chamber view. Longitudinal strain measurements are significantly reduced in the inferolateral wall segments (light pink and blue areas). In this patient, the light pink and blue areas in the inferolateral wall segments represent the extent of the myocardial infarction on regional myocardial function. One of the limitations is that it can be difficult to trace the endocardial borders related to the coarse trabeculations especially in systole. This could be based on volumetric 3-D acquisition or on 2-D-based 3-D reconstruction methods. Another problem is endocardial border detection that can be challenging in the low-resolution 3-D data sets. It has been used to study force–frequency relationships, which requires heart rate manipulation (stress echocardiography or pacing). The right upper is the coronal plane, the middle the transverse plane, and the lower the sagittal plane. Systolic Function of the Univentricular Heart With advances in surgical palliation of univentricular congenital heart disease, patients now survive longer and the single ventricle must support both the systemic and pulmonary circulations over many years. Functional evaluation of single ventricles is largely based on subjective assessment and no specific recommendations are available from any professional association. Tissue Doppler measurements and longitudinal strain measurements can also be obtained in this population. This is probably related to the chronic volume unloading related to the Fontan surgery and the absence of biventricular interactions. For all methods interpretation of results is affected by abnormal geometry, ventricular size, and loading conditions. Ventricular/Ventricular Interaction In congenital heart, the ventricular–ventricular interactions are important for both systolic and diastolic function assessment. Description of the septal position in systole and diastole should therefore be part of the assessment of cardiac function. How this is important for patients with congenital heart disease needs further exploration. The electrical interreaction between both ventricles is also very important as discussed further in the section on dyssynchrony evaluation. It is routine to perform a quantitative evaluation of the aortic structures from the level of the valve annulus through the distal aortic arch. Evaluation of the aortic root itself consists of 2-D assessment of the aortic annular dimension, dimension of the aorta at the level of the sinuses of Valsalva, and dimension of the sinotubular junction, ascending aorta, proximal and distal transverse aortic arch, and aortic isthmus. Therefore, aortic root dimensions are best assessed in the parasternal long axis with the proximal ascending aorta and aortic root perpendicular to the ultrasound beam. Different techniques for measuring the aortic root have been proposed and when using normal data, it is important to know which technique was used to establish the reference values. Measurements can be obtained during early to midsystole as suggested by the pediatric guidelines (3), but most of the normal reference papers have used diastolic measurements of the aortic root. The alternative technique is to measure the aortic root between the anterior and posterior inner edges. The aortic valve is magnified in the parasternal long-axis view and the annulus measured from the inner edge of the proximal valve insertion hinge point within the arterial root to the inner edge of the opposite hinge point (Fig. The sinus of Valsalva and sinotubular junction are also measured from the parasternal long-axis view. To visualize the aortic root and ascending aorta, it may be necessary to move the transducer one or two intercostal spaces higher (high left parasternal view). The ascending aorta is measured at the level where it crosses the right pulmonary artery. Imaging of the transverse arch and isthmus is usually done in long-axis images of the aortic arch from the suprasternal notch window. Measurements should be performed at the level of the proximal transverse arch (between the innominate and left carotid arteries), the distal transverse arch (between the left carotid and left subclavian arteries), and the aortic isthmus (the narrowest segment distal to the left subclavian artery). In this parasternal short-axis view, the pulmonary valve annulus is measured at the hinge point of the valve leaflets in early systole. The pulmonary valve is best measured from the parasternal long-axis outflow view, although it can also be measured from the parasternal short-axis view (lower resolution) (Fig. The main pulmonary artery can be measured between the sinotubular junction and the bifurcation. The proximal right pulmonary artery is best measured from the suprasternal view where it crosses behind the aorta. Semilunar Valve Stenosis Prior to measuring gradients, the level of obstruction needs to be determined by 2-D and color Doppler imaging. The severity of aortic and pulmonary valve stenosis in pediatric heart disease is based on Doppler measurement of the peak and mean transvalvular gradient. As with all Doppler assessments, interrogation of transvalvular flow jets should be performed with an angle of insonation as parallel to the direction of flow as possible to minimize underestimation of the valve gradient. As such, aortic valve gradients are most accurately assessed from either the apical window or from a high right parasternal window, with the ultrasound plane angled inferiorly toward the ascending aorta (Fig. For the pulmonary valve, the parasternal short- and long-axis views can be used and in infants and smaller children, subcostal imaging can be useful. The peak instantaneous Doppler velocity is measured and the gradient calculated using the Bernoulli equation. This is different from the peak-to-peak gradient measured in the cardiac catheterization laboratory by pullback of the P. The peak instantaneous pressure gradient is calculated from the peak instantaneous flow velocity that occurs across the semilunar valve at a single time point in systole. When peak-to-peak gradients are measured by pullback of the catheter in the cardiac catheterization laboratory, the gradient is expressed as the difference between the peak pressure upstream of the valve (or point of obstruction) and peak pressure proximal to the valve, which does not occur simultaneously in the cardiac cycle. The peak-to-peak gradient measured by echocardiography will often be higher compared to the peak-to-peak gradient measured by catheterization. Mean gradients correlate better with peak-to-peak gradients obtained in the catheterization laboratory. For the pulmonary valve, the peak instantaneous gradient correlates better with the peak-to-peak gradient on pullback—and this explains why for assessing severity of pulmonary valve stenosis, the peak instantaneous gradient is used—while for the aortic valve, the mean gradient is considered to better correlate with the peak-to-peak gradient. This position and view frequently affords the best Doppler alignment with the aortic stenosis jet.

Thus rate alone cannot be used to exclude potentials suspected of being generated by a ventilator order cheap zovirax on-line. Inadequate or unstable contact between the electrode surface and the skin may result in a sudden change in the junction potential and/or impedance that can produce extraneous potentials in affected channels generic zovirax 400 mg free shipping. These may appear as single or repetitive rapid buy zovirax with a visa, spike-like waves with an abrupt upward initial phase (the so-called P. Sources of artifacts that can mimic generalized activity that is either paroxysmal or sustained Instrumentation-patient interface ○ Spontaneous and passive movements ▪ Rocking, patting Instrumentation ○ Swaying of electrode leads Physiologic ○ Sweating Environment ○ 60-Hz interference from adjacent instruments The electrode interface also may be altered by the degree to which the infant may perspire. Diffuse sweating may result in long-duration potentials that initially appear as generalized or regional slow activity (Figs. Very slow potentials may occur because of changes caused by alterations in surface electrolyte compositions—these potentials are similar to the galvanic skin response. Movement of the head against the bed due to respirations or other body movements may produce sharp and/or slow potentials arising from that particular electrode (Figs. Pulse also may cause a recorded artifact by production of movement in a region adjacent to an electrode site. This is owing to a mechanical, or ballistic, movement induced by the instrument—a cause of artifact from these devices different from electrical interference described earlier. Other body movements also may alter the patient-electrode interface and result in artifacts. These include limb movements that may be random, purposeful, or associated with clinical seizures and other limb or body movements (Figs. Movements created to comfort the infant, such as rocking and patting the infant, may be particularly troublesome. Digital recordings may have problems relating to malfunction of the operating system. The edema may be the result of transit through the birth canal, more significant birth or other trauma, placement of intravenous lines with or without extravasation of fluid, the placement of a ventriculoperitoneal shunt, or the presence of a surgical wound. Diffuse edema may lead to a pattern of background activity that is low in amplitude in all regions. Regional or asymmetric edema may lead to a pattern of focal depression, suggesting a focal lesion if the edema is not noted. Conductive properties may be altered because of the absence of underlying skull, typically (although rarely) in the case of cranial surgery. Respirations also may appear as artifacts, whether they are spontaneous or driven by a ventilator. These artifacts may be unilateral or bilateral, depending on body and head position. These movements include oral-buccal-lingual movements, such as sucking and tongue thrusting (i. Periodic electrical interference due to mechanical device Alternations of Electrode Impedance Fig. Sustained, high-amplitude, long-duration potentials due to sweat Induced by Movements Fig. Moderately high-amplitude, short-duration, repetitive potentials due to head movement associated with sobbing Fig. High-amplitude generalized spike-like artifact associated with generalized myoclonic movement Fig. Rhythmic sharp wave activity induced by patting Endogenous Noncerebral Potentials Fig. Electrical interference is present in all leads when an infusion pump for intravenous fluids is activated at the bedside. Electrical artifact is present in channels involving the C3 electrode, which has relatively high impedance compared with others. The Pz electrode in this recording has become unstable, resulting in irregular, sustained, low-voltage, relatively fast activity. The high- voltage, long-duration waveforms are predominantly in frontal and central regions and are sustained. The electrocardiogram also is reflected in leads from the left central region and there is electromyographic activity in the anterior leads. Moderately high-amplitude, short- duration, repetitive potentials due to head movement associated with sobbing. This infant experienced a brief sobbing episode characterized by shuddering that involved respiration and truncal muscles as well as head, which was turned to the right. The simultaneous body movements are indicated by waveforms in the electromyogram channel. High-amplitude generalized spike-like artifact associated with generalized myoclonic movement. High-voltage rhythmic theta activity is present with variable localization and is preceded and followed by high-voltage, very slow activity. This movement is marked by the generalized high-amplitude slow activity in the middle of this segment. Although associated with sucking, this activity is not produced by endogenous potentials, but rather by movement of the head that occurs in conjunction with the vigorous sucking movements. A brief run of slow activity in the right frontal region aligns with the activity recorded in the electroculogram channel. Rhythmic, slow, sharp waves are present in the frontal regions bilaterally, higher in amplitude on the left, aligned with the recorded electrooculogram and occurring in association with clinically observed nystagmus. High-voltage, slow activity is present in the frontal regions bilaterally associated with rhythmic eye opening and closure. Visual analysis and interpretation require determination of the degree of continuity of background activity (Fig. They also require recognition of specific wave forms and patterns that occur with increasing age (Fig. Temporal alpha bursts replace 4- to 5-Hz bursts (33 wk) 34-35 C D C +++ + +++ No 1. Continuous bioccipital R delta activity with superimposed 12- to 15- Hz activity during active sleep 2. The voltage of the fast activity varies throughout each burst but rarely exceeds 75 μV. Various names have been given to these complexes: “spindle-delta bursts,” “brushes,” “spindle-like fast waves,” and “ripples of prematurity. An important feature of beta-delta complexes is that they typically occur asynchronously in derivations from homologous areas and show a variable voltage asymmetry on the two sides. During the next 5 to 6 weeks, they become progressively more persistent, and the voltage of the fast component usually increases. Temporal Theta and Alpha Bursts A useful developmental marker is the appearance of rhythmic 4 to 6-Hz waves occurring in short bursts of rarely more than 2 seconds, arising independently in the left and right midtemporal areas. Individual waves may often have a sharp configuration (Hughes, 1987; Werner et al.

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