The decrease in cerebrovascular resistance during NMS indicates that the integrity of cerebrovascular autoregulation is maintained even when syncope is imminent. The selective loss of diastolic flow during syncope and the increase in pulsatility index are likely caused by collapse of downstream vessels as diastolic blood pressure decreases below the critical closing pressure of cerebral vessels.

To test whether cerebral autoregulation is impaired in patients with neurally mediated syncope (NMS), we evaluated 15 normal subjects and 37 patients with recurrent NMS. Blood pressure (BP), heart rate, and cerebral blood velocity (CBV) (transcranial Doppler) were recorded at rest and during 80 degrees head-up tilt (HUT). Static cerebral autoregulation as assessed from the change in cerebrovascular resistance during HUT was the same in NMS and controls. Properties of dynamic cerebral autoregulation were inferred from transfer gain, coherence, and phase of the relationship between BP and CBV estimated from filtered data segments (0.02-0.8 Hz). During the 3 min preceding syncope, dynamic cerebral autoregulation of subjects with NMS did not differ from that of controls nor did it change over the course of HUT in patients with NMS or in control subjects. Dynamic cerebral autoregulation was also unaffected by the degree of orthostatic intolerance as inferred from latency to onset of syncope. We conclude that cerebral autoregulation in patients with recurrent syncope does not differ from that of normal control subjects.

No abstract

Vol. 37, No.2, 1995 Primed in U.S.A.The purpose of this study was to evaluate the visual development of preterm infants from 1 to 6 mo of age, using the pattern visual evoked potentials (VEP) in response to three check sizes: 60, 30, and 15 min of arc. Pattern YEP were recorded in 24 full-term and 24 preterm infants (26-36 wk of gestation). The results showed a rapid visual maturation between 1 and 3 mo, followed by a slower progression over the next 3 mo, in both groups. The implicit time of the PlOOwave of the pattern YEP was also found to shorten with increasing check sizes. The maturation of pattern YEP in preterm infants was shown to be related to their gestational (or corrected) age rather than their Preterm infants are know n to be at risk for a numb er of vision-threatening conditions such as intraventricular hemorrhage (1), perinatal cerebral hypoxia (2), and retin opathy of prematurity (3), which can alter the normal maturation of the visual syste m. Studies (4 -13) have been conducted to determine the time course of the norm al visual development in preterm infants compared with full-t erm infants. Preterm infant s are exposed to visual stimulation for an additional period of several weeks or month s in comp arison with infants born after the normal 40 wk of gestation , and this precocious expe rience could have an effect on the dev elopmental rate of visual functions. The results reported on the influen ce of visual experience versus the maturation of the visual system are often contradictory.Earlier studies on preterm infants using behavioral methods (4-8) sugges ted that the extrav isual experience wo uld not influence the development of visual acuity, which appeared to be related to the infant' s ges tational (or corre cted) age rather than its postnatal age. More recent reports using eithe r the steady-state YEP testin g (9) or preferential looking method (10-11) reve aled that the developm ent of visual ac uity in Received October 11, 1993; accepted August 23, 1994. Correspondence: Dr. Marie-Sylvie Roy, Department of Ophthalmology, Hopital SainteJustine, 3175, Cote Ste. Catherine Road, Montreal, Quebec, Canada H3T l C5.Supported by a grant from FORMOEIL (Fondation pour la recherche sur les maladies de l'Oeil) and FRSQ 930214-103 from the Fonds de la recherc he en sante du Quebec. postnatal age. The pattern YEP obtained in response to a 60-min check size in preterm infants aged between 1.5 and 2.5 mo (corrected age) showed a tendency for a faster maturation than those of full-term infants. Our results suggest that within the first 6 mo of age, pattern YEP response is useful to monitor visual development in full-term infants as well as in preterm infants using corrected age. (Pediatr Res 37: 140-144, 1995) Abbreviations YEP, visual evoked potential ANOVA, analysis of variance health y preterm infan ts wo uld be acce lera ted when compared with full-term infants. If there is an accelerating or facilitating effect in preterm infants resulting from an extrauterine experience before the ...

Previous studies have shown that newborn rats exposed postnatally to hyperoxia will develop a permanent impairment of the retinal function as determined with the electroretinogram (ERG). The purpose of our study was to examine whether postnatal hyperoxia equally alters the light- and dark-adapted ERGs and oscillatory potentials (OPs) as well as leads to permanent structural modification of the retina. During the first 14 days of life, cohorts of Sprague-Dawley rats were exposed to a hyperoxic environment, and ERGs were recorded at mean ages of approximately 25 and 55 days. Our results indicate that both light- and dark-adapted ERGs and OPs are already significantly altered within a few days following exposure to hyperoxia. None of the ERG and (or) OP parameters, with the exception of the a-wave, returned to normal values by 55 days of age. In fact some dark-adapted OPs were completely abolished following postnatal O2 exposure. Histological analysis revealed that the retina of rats exposed to hyperoxia failed to develop an outer plexiform layer and had a reduced count of horizontal cells, consistent with the permanent postreceptoral anomalies seen in the ERG responses. Our results suggest that postnatal hyperoxia causes a generalized retinal disorder leading to permanent structural modifications of the retinal cytoarchitecture and lasting anomalies of the rod and cone functions.

autoregulation is preserved in postural tachycardia syndrome. J Appl Physiol 99: 828 -835, 2005. First published April 28, 2005 doi:10.1152/japplphysiol.00225.2005.-To test whether cerebral autoregulation is impaired in patients with postural tachycardia syndrome (POTS), we evaluated 17 healthy control subjects and 27 patients with POTS. Blood pressure, heart rate, and cerebral blood velocity (transcranial Doppler) were recorded at rest and during 80°h ead-up tilt (HUT). Static cerebral autoregulation, as assessed from the change in cerebrovascular resistance during HUT, was the same in POTS and in controls. The properties of dynamic cerebral autoregulation were inferred from transfer gain, coherence, and phase of the relationship between blood pressure and cerebral blood velocity estimated from filtered data segments (0.02-0.8 Hz). Dynamic cerebral autoregulation of patients with POTS did not differ from that of controls. The patients' dynamic cerebral autoregulation did not change over the course of HUT, despite increased tachycardia suggestive of worsening orthostatic stress. Inflation of military anti-shock trouser pants substantially reduced the tachycardia of patients with POTS without affecting cerebral autoregulation. Symptoms of orthostatic intolerance were reduced in one-half of the patients following military anti-shock trouser pants inflation. We conclude that cerebral perfusion and autoregulation in many patients with POTS do not differ from that of normal control subjects. cerebrovascular circulation; Fourier analysis; hemodynamics THE POSTURAL ORTHOSTATIC TACHYCARDIA syndrome (POTS) is a form of orthostatic intolerance that is characterized by symptoms of lightheadedness, fatigue, palpitations, diminished concentration, blurred vision, tremulousness, shortness of breath, nausea, and impaired cognition that mainly occur during upright posture (5,24,31,33). To qualify for the diagnosis of POTS, these symptoms must occur in conjunction with an increase in heart rate (HR) of Ͼ30 beats/min or a HR Ͼ 120 beats/min within the first 5 min of standing (23)(24)(25)31). The HR increase should be sustained and not associated with orthostatic hypotension (46). Many patients have evidence of hypovolemia (16,26) or exaggerated venous pooling with central hypovolemia (32,48). Inflation of military anti-shock trousers (MAST pants), which prevent venous pooling in the legs, usually causes reversal of the tachycardia (49). The pathophysiology of POTS is poorly understood. Various abnormalities have been described, including the presence of an attenuated autonomic neuropathy (25, 43), increased cardiac norepinephrine spillover (19), impaired norepinephrine transporter (45), or reduced vagal cardiac baroreflex sensitivity (14). Some patients may have evidence of increased sympathetic activity while supine (17, 18), whereas others do not (5).Regardless of pathophysiology, all patients with POTS are significantly disabled by the constellation of symptoms noted above (2).Lightheadedness and impaired concentration while ...

Many of the primary symptoms of orthostatic intolerance (fatigue, diminished concentration) as well as some of the premonitory symptoms of neurally mediated syncope (NMS) are thought to be due to cerebral hypoperfusion. Transcranial Doppler measurements of middle cerebral artery blood velocity (CBV) is at present the only technique for assessing rapid changes in cerebral blood flow, and hence for evaluating dynamic cerebral autoregulation. However, controversies exist regarding data interpretation. At syncope, during the collapse of blood pressure (BP), diastolic CBV diminishes, whereas systolic CBV is maintained. Some consider this increase in CBV pulsatility to be indicative of a paradoxical increase in cerebrovascular resistance (CVR) prior to syncope. Others note that mean CBV decreases much less than does mean BP, implying that cerebral autoregulatory mechanisms are intact and functioning at syncope. Similarly, there is no evidence of impaired dynamic cerebral autoregulation, as measured by standard linear transfer‐function analysis, in patients with NMS. Some patients with exaggerated postural tachycardia (POTS) have been found to have an excessive decrease in CBV during head‐up tilt. Controversy exists as to whether this decrease results from an excessive sympathetic outflow to the cerebral vasculature or from hyperventilation. However, many other equally symptomatic patients with a similar hemodynamic profile of exaggerated tachycardia during head‐up tilt have normal CBV changes during this maneuver and have normal dynamic cerebral autoregulation as determined by transfer‐function analysis. Whether these discrepancies reflect different pathologies in patients with POTS is currently unknown.

Previous studies have shown that newborn rats exposed postnatally to hyperoxia will develop a permanent impairment of the retinal function as determined with the electroretinogram (ERG). The purpose of our study was to examine whether postnatal hyperoxia equally alters the light- and dark-adapted ERGs and oscillatory potentials (OPs) as well as leads to permanent structural modification of the retina. During the first 14 days of life, cohorts of Sprague-Dawley rats were exposed to a hyperoxic environment, and ERGs were recorded at mean ages of approximately 25 and 55 days. Our results indicate that both light- and dark-adapted ERGs and OPs are already significantly altered within a few days following exposure to hyperoxia. None of the ERG and (or) OP parameters, with the exception of the a-wave, returned to normal values by 55 days of age. In fact some dark-adapted OPs were completely abolished following postnatal O2 exposure. Histological analysis revealed that the retina of rats exposed to hyperoxia failed to develop an outer plexiform layer and had a reduced count of horizontal cells, consistent with the permanent postreceptoral anomalies seen in the ERG responses. Our results suggest that postnatal hyperoxia causes a generalized retinal disorder leading to permanent structural modifications of the retinal cytoarchitecture and lasting anomalies of the rod and cone functions.