Brain Autoregulation Research Articles

Prediction of poor prognosis using the peak systolic velocity and early diastolic velocity of the central retinal artery in patients with post‐cardiac arrest syndrome

AbstractIntroductionMonitoring intracranial pressure (ICP) in patients with post‐cardiac arrest syndrome (PCAS) is crucial for effective management and prognosis assessment. However, continuous ICP monitoring is rarely practiced. Increased ICP is often associated with the impairment of brain autoregulation. This study investigated whether central retinal artery (CRA) flow velocity, autoregulation status according to mean arterial pressure (MAP), and the optic nerve sheath diameter (ONSD)/eyeball transverse diameter (ETD) ratio could predict poor prognosis related to increased ICP in PCAS patients.MethodsIn this multicenter prospective observational study, transocular ultrasonography of the optic nerve sheath was performed on 38 PCAS patients treated with targeted temperature management from December 2021 to November 2022. CRA peak systolic velocity (PSV), early diastolic velocity (eDV), MAP, CRA‐PSV changes following MAP changes (autoregulation), and ONSD/ETD ratio were measured repeatedly from days 0 to 4 post‐admission.ResultsUnivariable analysis indicated that CRA‐PSV, nonpositive or flat CRA‐eDV, and disrupted autoregulation correlated with a poor prognosis (Cerebral Performance Category 4 or 5). In multivariable analysis, nonpositive CRA‐eDV or disrupted autoregulation was the most significant predictor of poor prognosis (odds ratio, 40.576; p = 0.002), with an area under the curve of 0.774. The ONSD/ETD ratio did not show a significant correlation.ConclusionsNonpositive CRA‐eDV, CRA‐PSV and disrupted autoregulation can predict poor prognosis in PCAS patients. Transocular Doppler ultrasonography of the CRA and autoregulation assessment may aid in ICP monitoring and management in PCAS patients.

Alterations in Regional Brain Microcirculation in Patients with Sepsis: A Prospective Study Using Contrast-Enhanced Brain Ultrasound.

Alterations in regional brain microcirculation have not been well studied in patients with sepsis. Regional brain microcirculation can be studied using contrast-enhanced brain ultrasound (CEUS) with microbubble administration. CEUS was used to assess alterations in regional brain microcirculation on 3 consecutive days in 58 patients with sepsis and within 24h of intensive care unit admission in 10 aged-matched nonseptic postoperative patients. Time-intensity perfusion curve variables (time-to-peak and peak intensity) were measured in different regions of interest of the brain parenchyma. The mean arterial pressure, cardiac index (using transthoracic echocardiography), global cerebral blood flow (using echo-color Doppler of the carotid and vertebral arteries), mean flow velocities of the middle cerebral arteries, and brain autoregulation (using transcranial echo-color Doppler) were measured simultaneously. The presence of structural brain injury in patients with sepsis was confirmed on computed tomography imaging, and encephalopathy, including coma and delirium, was evaluated using the Glasgow Coma Scale and the Confusion Assessment Method in the Intensive Care Unit. Of the 58 patients with sepsis, 42 (72%) developed acute encephalopathy and 11 (19%) had some form of structural brain injury. Brain autoregulation was impaired in 23 (40%) of the patients with sepsis. Brain microcirculation alterations were observed in the left lentiform nucleus and left white matter of the temporoparietal region of the middle cerebral artery in the sepsis nonsurvivors but not in the survivors or postoperative patients. The alterations were characterized by prolonged time-to-peak (p < 0.01) and decreased peak intensity (p < 0.01) on the time-intensity perfusion curve. Prolonged time-to-peak but not decreased peak intensity was independently associated with worse outcome (p = 0.03) but not with the development of encephalopathy (p = 0.77). Alterations in regional brain microcirculation are present in critically ill patients with sepsis and are associated with poor outcome. Trial registration Registered retrospectively on December 19, 2019.

Monitoring Mean Arterial Preasur (MAP) in Traumatic Brain Injury Patients during The Initial 60 Minutes of Manitol 20%

The effect of manitol 20% on changes in blood pressure after traumatic brain injury is unknown. The purpose of this study was to analyze the differences in blood pressure before and after the administration of 20% mannitol in traumatic brain injury patients at the Intensive Care Unit. This study is a quasi experimental research which uses a pre-post test without control one group design, a method used in observational analytic techniques. The population of this study were all traumatic brain injury patients who were given a manitol infusion of 20% 100ml, with consecutive sampling technique, obtained 12 samples. With a significance threshold of p 0.05, the test was performed using the Paired T test on systolic and MAP data and the post hoc Wilcoxon test on diastolic data.  paired t-test systolic p=0.000, MAP p=0,000. Wilcoxon test diastolic p=0,002. Decreasing blood pressure 15 minutes after administration of 20% mannitol occurs because half live mannitol which lowers blood pressure and responds to decreased blood pressure autoregulation, at 30 minutes resulting in decreased intra-cranial pressure, improves cerebral perfusion and brain autoregulation that affects systemic blood pressure 60 changes in blood pressure may be due to diuresis effects. During the administration of mannitol there is a change in blood pressure that needs to be monitored

Can a Therapeutic Strategy for Hypotension Improve Cerebral Perfusion and Oxygenation in an Experimental Model of Hemorrhagic Shock and Severe Traumatic Brain Injury?

Restoration of brain tissue perfusion is a determining factor in the neurological evolution of patients with traumatic brain injury (TBI) and hemorrhagic shock (HS). In a porcine model of HS without neurological damage, it was observed that the use of fluids or vasoactive drugs was effective in restoring brain perfusion; however, only terlipressin promoted restoration of cerebral oxygenation and lower expression of edema and apoptosis markers. It is unclear whether the use of vasopressor drugs is effective and beneficial during situations of TBI. The objective of this study is to compare the effects of resuscitation with saline solution and terlipressin on cerebral perfusion and oxygenation in a model of TBI and HS. Thirty-two pigs weighing 20-30kg were randomly allocated into four groups: control (no treatment), saline (60ml/kg of 0.9% NaCl), terlipressin (2mg of terlipressin), and saline plus terlipressin (20ml/kg of 0.9% NaCl + 2mg of terlipressin). Brain injury was induced by lateral fluid percussion, and HS was induced through pressure-controlled bleeding, aiming at a mean arterial pressure (MAP) of 40mmHg. After 30min of circulatory shock, resuscitation strategies were initiated according to the group. The systemic and cerebral hemodynamic and oxygenation parameters, lactate levels, and hemoglobin levels were evaluated. The data were subjected to analysis of variance for repeated measures. The significance level established for statistical analysis was p < 0.05. The terlipressin and saline plus terlipressin groups showed an increase in MAP that lasted until the end of the experiment (p < 0.05). There was a notable increase in intracranial pressure in all groups after starting treatment for shock. Cerebral perfusion pressure and cerebral oximetry showed no improvement after hemodynamic recovery in any group. The groups that received saline at resuscitation had the lowest hemoglobin concentrations after treatment. The treatment of hypotension in HS with saline and/or terlipressin cannot restore cerebral perfusion or oxygenation in experimental models of HS and severe TBI. Elevated MAP raises intracranial pressure owing to brain autoregulation dysfunction caused by TBI.

Wanita Usia 39 Tahun dengan Ensefalopati Hipertensi: Laporan Kasus

Hypertensive encephalopathy is an acute reversible syndrome caused by a sudden increase of blood pressure so crosses the limits of brain auto-regulation. The objective of writing this scientific paper was to present clinical manifestations of hypertensive encephalopathy and report the favorable clinical outcomes in hypertensive encephalopathy patients with comprehensive therapy. This paper is an empirical case study investigates the symptoms of Hypertensive Encephalopathy in real life. Female, 39 years old complaints of sudden seizures, before the seizure she felt of non-throbbing headache all over her head. There was an increase in blood pressure of 200/130 mmHg. On neurologic-ophthalmologic examination, her right eye had no light perception (NLP), while on other neurological functions there were no abnormalities. She was hospitalized and treated with antihypertensive drugs, that are Amlodipine and Lamipril, during inpatient the DASH diet was given. The patient showed improvement, then was discharged on the 5th day of treatment. Diagnosis of hypertensive encephalopathy was made in this patient built upon high blood pressure plus neurologic symptoms and the exclusion of other conditions that could cause similar symptoms. Antihypertensives were used carefully at a target blood pressure of 150/100 mmHg (20% of MAP). Application of DASH diet has an effect for lowering blood pressure due to the restriction of sodium intake from food. Management of hypertensive encephalopathy includes lowering blood pressure but it’s not recommended aggressively because it can cause ischemia. Preventive measures are very important, research is needed on predictive factors for hypertension encephalopathy and a high level of alertness in risk groups.

Study of the relationship between regional cerebral saturation and pCO2 changes during mechanical ventilation to evaluate modifications in cerebral perfusion in a newborn piglet model.

Near-infrared spectroscopy (NIRS) could be a useful continuous, non-invasive technique for monitoring the effect of partial pressure of carbon dioxide (PaCO2) fluctuations in the cerebral circulation during ventilation. The aim of this study was to examine the efficacy of NIRS to detect acute changes in cerebral blood flow following PaCO2 fluctuations after confirming the autoregulation physiology in piglets. Fourteen piglets (<72 h of life) were studied. Mean arterial blood pressure, oxygen saturation, pH, glycemia, hemoglobin, electrolytes, and temperature were monitored. Eight animals were used to evaluate brain autoregulation, assessing superior cava vein Doppler as a proxy of cerebral blood flow changing mean arterial blood pressure. Another 6 animals were used to assess hypercapnia generated by decreasing ventilatory settings and complementary CO2 through the ventilator circuit and hypocapnia due to increasing ventilatory settings. Cerebral blood flow was determined by jugular vein blood flow by Doppler and continuously monitored with NIRS. A decrease in PaCO2 was observed after hyperventilation (47.6±2.4 to 29.0±4.9 mmHg). An increase in PaCO2 was observed after hypoventilation (48.5±5.5 to 90.4±25.1 mmHg). A decrease in cerebral blood flow after hyperventilation (21.8±10.4 to 15.1±11.0 mL/min) and an increase after hypoventilation (23.4±8.4 to 38.3±10.5 mL/min) were detected by Doppler ultrasound. A significant correlation was found between cerebral oxygenation and Doppler-derived parameters of blood flow and PaCO2. Although cerebral NIRS monitoring is mainly used to detect changes in regional brain oxygenation, modifications in cerebral blood flow following experimental PaCO2 changes were detected in newborn piglets when no other important variables were modified.

Applications and Limitations of Neuro-Monitoring in Paediatric Anaesthesia and Intravenous Anaesthesia: A Narrative Review.

Safe management of anaesthesia in children has been one of the top areas of research over the last decade. After the large volume of articles which focused on the putative neurotoxic effect of anaesthetic agents on the developing brain, the attention and research efforts shifted toward prevention and treatment of critical events and the importance of peri-anaesthetic haemodynamic stability to prevent negative neurological outcomes. Safetots.org is an international initiative aiming at raising the attention on the relevance of a high-quality anaesthesia in children undergoing surgical and non-surgical procedures to guarantee a favourable outcome. Children might experience hemodynamic instability for many reasons, and how the range of normality within brain autoregulation is maintained is still unknown. Neuro-monitoring can guide anaesthesia providers in delivering optimal anaesthetic drugs dosages and also correcting underling conditions that can negatively affect the neurological outcome. In particular, it is referred to EEG-based monitoring and monitoring for brain oxygenation.

Influence of cerebral hyperthermia on intracranial pressure and autoregulation of cerebral circulation in patients with acute brain injury

To study the effect of hyperthermia on intracranial pressure (ICP) and cerebral autoregulation (Prx). There were 8 patients with acute brain injury, signs of brain edema and intracranial hypertension. Cerebral autoregulation was assessed by using of PRx. ICP, CPP, BP, PRx were measured before and during hyperthermia. We have analyzed 33 episodes of cerebral hyperthermia over 38.30 C. Statistica 10.0 (StatSoft) was used for statistical analysis. Only ICP was significantly increased by 6 [3; 11] mm Hg (p<0.01). In patients with initially normal ICP, hyperthermia resulted increase of ICP in 48% of cases (median 24 [22; 28] mm Hg). In patients with baseline intracranial hypertension, progression of hypertension was noted in 100% cases (median 31 [27; 32] mm Hg) (p<0.01). Hyperthermia resulted intracranial hypertension regardless brain autoregulation status. Cerebral hyperthermia in patients with initially normal ICP results intracranial hypertension in 48% of cases. In case of elevated ICP, further progression of intracranial hypertension occurs in 100% of cases. Cerebral hyperthermia is followed by ICP elevation in both intact and impaired cerebral autoregulation.

Delayed Ischemic Neurologic Deficit after Aneurysmal Subarachnoid Hemorrhage.

Delayed ischemic neurologic deficit (DIND) is the main preventable cause of poor outcomes in aneurysmal subarachnoid hemorrhage (SAH) patients. Of 50% of survivors from a SAH, approximately 30% of patients will present clinical vasospasm (VS). The cornerstone of the DIND management comprises prevention and early identification. Several diagnostic methods have been proposed differing in efficacy, invasiveness, and costs. Serial neurological examination is the most reliable method to detect a new neurological deficit. On the other hand, comatose patients require advanced monitoring methods which identify changes in the microcirculatory environment, brain autoregulation, and spreading depolarization. Multimodality monitoring with continuous electroencephalography, microdialysis, and intracranial pressure monitoring represents altogether the current state-of-art technology for the intensive care of SAH patients. Moreover, advances in genetic biomarkers to predict clinical VS have shown consistent accuracy which may in the near future allow the early prediction of DIND through a simple blood test. Several clinical trials have tested drugs with theoretical effects on DIND prevention or treatment. Nevertheless, nimodipine remains the Holy Grail in the prevention of clinical VS. Among rescue therapies, the endovascular treatment through intra-arterial vasodilator (verapamil or nicardipine) infusion is the most employed method for DIND reversal; however, there is no good quality evidence comparing results of intra-arterial infusion of vasodilators versus balloon angioplasty. Although we have addressed the most refined technology in the management of SAH and DIND, the clinical experience and strict follow-up in neurointensive care will be determinant for favorable long-term outcomes.

Role of flow velocity and transient hyperemic response evaluated by transcranial doppler for assesing brain autoregulation in mild traumatic brain injury: a case report

Role of flow velocity and transient hyperemic response evaluated by transcranial doppler for assesing brain autoregulation in mild traumatic brain injury: a case report

Small vessel disease to subcortical dementia: a dynamic model, which interfaces aging, cholinergic dysregulation and the neurovascular unit.

BackgroundSmall vessels have the pivotal role for the brain’s autoregulation. The arteriosclerosis-dependent alteration of the brain perfusion is one of the major determinants in small vessel disease. Endothelium distress can potentiate the flow dysregulation and lead to subcortical vascular dementia (sVAD). sVAD increases morbidity and disability. Epidemiological studies have shown that sVAD shares with cerebrovascular disease most of the common risk factors. The molecular basis of this pathology remains controversial.PurposeTo detect the possible mechanisms between small vessel disease and sVAD, giving a broad vision on the topic, including pathological aspects, clinical and laboratory findings, metabolic process and cholinergic dysfunction.MethodsWe searched MEDLINE using different search terms (“vascular dementia”, “subcortical vascular dementia”, “small vessel disease”, “cholinergic afferents”, etc). Publications were selected from the past 20 years. Searches were extended to Embase, Cochrane Library, and LILIACS databases. All searches were done from January 1, 1998 up to January 31, 2018.ResultsA total of 560 studies showed up, and appropriate studies were included. Associations between traditional vascular risk factors have been isolated. We remarked that SVD and white matter abnormalities are seen frequently with aging and also that vascular and endothelium changes are related with age; the changes can be accelerated by different vascular risk factors. Vascular function changes can be heavily influenced by genetic and epigenetic factors.ConclusionSmall vessel disease and the related dementia are two pathologies that deserve attention for their relevance and impact in clinical practice. Hypertension might be a historical problem for SVD and SVAD, but low pressure might be even more dangerous; CBF regional selective decrease seems to be a critical factor for small vessel disease-related dementia. In those patients, endothelium damage is a super-imposed condition. Several issues are still debatable, and more research is needed.

Perspective: Variation in Guideline Implementation and Adherence Regarding Severe Traumatic Brain Injury Treatment: A CENTER-TBI Survey Study in Europe

Since 1990, the so-called “Brain Decade” was an exciting and promising period for the comprehension and tentative of treatment of the head trauma in order to improve the outcome of those devastating pathology.After several research and pre-clinical and clinical results a lot of protocols started with the concepts of brain autoregulation, brain perfusion, and neural rescue. Brain monitoring, also with the multimodal approach, transcranial Doppler, hypothermia, and neurosurgical techniques for brain decompression were also again updated.In 1992, the Lund protocol (LP) was the first guide published in Europe, for treatment of severe traumatic brain injury (s-TBi) (Grande, 2017). It was a theoretical approach in the field of brain pathophysiology. The main idea was on the way of cerebral perfusion pressure, fluid therapy, ventilation, sedation, nutrition, the use of vasopressors, and osmotherapy. The treatment is standardized, strictly applied with less need for individualization of the patient. Alternative European guidelines were published a few years later and were mainly based on meta-analytic approaches from clinical outcome studies. When introduced, they differed extensively from the LP. We still lack any large randomized outcome study comparing the European guidelines with other guidelines including the LP. From our point of view, there is poor evidence in favor of any of the guidelines used today. Despite the LP has not been changed since its introduction some components of the alternative guidelines have been proposed. As part of the “lucky Generation” of Neuroscientists, witnesses of the brain care evolution changing paradigms and evidence-based medicine era, in this chapter, we analyze and discuss the contents, results, and adherence of the current European protocols for head trauma.

Estimation of cerebral metabolic rate of oxygen consumption using combined multiwavelength photoacoustic microscopy and Doppler microultrasound.

The metabolic rate of oxygen consumption is an important metric of tissue oxygen metabolism and is especially critical in the brain, yet few methods are available for measuring it. We use a custom combined photoacoustic-microultrasound system and demonstrate cerebral oxygen consumption estimation in vivo. In particular, the cerebral metabolic rate of oxygen consumption was estimated in a murine model during variation of inhaled oxygen from hypoxia to hyperoxia. The hypothesis of brain autoregulation was confirmed with our method even though oxygen saturation and flow in vessels changed.

Genetic interference with peroxisome proliferator-activated receptor γ in smooth muscle enhances myogenic tone in the cerebrovasculature via A Rho kinase-dependent mechanism.

Myogenic responses by resistance vessels are a key component of autoregulation in brain, thus playing a crucial role in regulating cerebral blood flow and protecting the blood-brain barrier against potentially detrimental elevations in blood pressure. Although cerebrovascular disease is often accompanied by alterations in myogenic responses, mechanisms that control these changes are poorly understood. Peroxisome proliferator-activated receptor γ has emerged as a regulator of vascular tone. We hypothesized that interference with peroxisome proliferator-activated receptor γ in smooth muscle would augment myogenic responses in cerebral arteries. We studied transgenic mice expressing a dominant-negative mutation in peroxisome proliferator-activated receptor γ selectively in smooth muscle (S-P467L) and nontransgenic littermates. Myogenic tone in middle cerebral arteries from S-P467L was elevated 3-fold when compared with nontransgenic littermates. Rho kinase is thought to play a major role in cerebrovascular disease. The Rho kinase inhibitor, Y-27632, abolished augmented myogenic tone in middle cerebral arteries from S-P467L mice. CN-03, which modifies RhoA making it constitutively active, elevated myogenic tone to ≈60% in both strains, via a Y-27632-dependent mechanism. Large conductance Ca(2+)-activated K(+) channels (BKCa) modulate myogenic tone. Inhibitors of BKCa caused greater constriction in middle cerebral arteries from nontransgenic littermates when compared with S-P467L. Expression of RhoA or Rho kinase-I/II protein was similar in cerebral arteries from S-P467L mice. Overall, the data suggest that peroxisome proliferator-activated receptor γ in smooth muscle normally inhibits Rho kinase and promotes BKCa function, thus influencing myogenic tone in resistance arteries in brain. These findings have implications for mechanisms that underlie large- and small-vessel disease in brain, as well as regulation of cerebral blood flow.

Kidney-brain link in traumatic brain injury patients? A preliminary report.

Kidney hyperfiltration with augmented renal clearance is frequently observed in patients with traumatic brain injury. The aim of this study is to report preliminary findings about the relationship between brain autoregulation impairment, estimated kidney glomerular filtration rate and outcome in critically ill patients after severe traumatic brain injury. Data collected from a cohort of 18 consecutive patients with severe traumatic brain injury managed with ICP monitoring in a Neurocritical Care Unit, were retrospectively analyzed. Early morning blood tests were performed for routine chemistry assessments and we analyzed creatinine and estimated creatinine clearance, osmolarity, and sodium. Daily norepinephrine dose, protein intake, and water balance were documented. Time average of brain monitoring data (intracranial pressure, cerebral perfusion pressure, and cerebrovascular reactivity pressure index--PRx) were calculated for 6 h before blood sample tests. Patient outcome was evaluated using Glasgow outcome scale at 6-month follow-up, considering nonfatal outcome if GOS ≥ 3 and fatal outcome if GOS < 3. Multiple linear regression models were used to study the crude and adjusted effects of the above variables on PRx throughout time. A total of 199 complete daily observations from 18 adult consecutive multiple trauma patients with severe traumatic brain injury were analyzed. At hospital admission, the median post-resuscitation Glasgow coma score was 6 (range 3-12), mean SAPSII score was 44.65 with predicted mortality of 36 %. Hospital mortality rate was 27 % and median GOS at 6 month after discharge was 3. Creatinine clearance (CrCl) was found to have a negative correlation with PRx (Pearson correlation--0.82), with statistically significant crude (p < 0.001) and adjusted (p = 0.001) effects. For each increase of 10 ml/min in CrCl (estimated either by the Cockcroft-Gault or by Modification of Diet in Renal Disease Study equations) a mean decrease in PRx of approximately 0.01 was expected. Amongst possible confounders only norepinephrine was shown to have a significant effect. Mean PRx value for outcome fatal status was greater than mean PRx for nonfatal status (p < 0.05), regardless of the model used for the CrCl estimation. Better cerebral autoregulation evaluated with cerebrovascular PRx is significantly correlated with augmented renal clearance in TBI patients and associates with better outcome.

The effect of maternal supine position on umbilical and cerebral blood flow indices

ObjectiveThe brain sparing phenomenon in the fetus is a protective mechanism aimed at maintaining sufficient blood flow towards the brain during chronic or acute fetal stress, such as that caused by hypoxemia or utero-placental insufficiency. In this study we investigated whether the brain sparing effect can also be elicited by a physiological stress associated with maternal posture.Study design Twenty-three low-risk pregnant women participated in the study. Between 36 and 40 weeks’ gestation, Doppler flow velocity waveforms were obtained from the fetal middle cerebral and the umbilical artery in the supine and the left lateral decubitus positions. Pulsatility index, systolic/diastolic index, and peak systolic velocities were measured and comparison was made between the left lateral and supine positions. ResultsThe pulsatility index in the middle cerebral artery decreased from 1.78±0.27 in the left lateral decubitus position to 1.29±0.16 in supine position (p<0.0001). Peak systolic velocity decreased from 46.05±7.85cm/s to 39.43±7.95cm/s, respectively (p=0.001). The pulsatility index in the umbilical artery decreased from 0.89±0.13 in the left lateral position to 0.74±0.11 in the supine position (p<0.0001). ConclusionsThis study demonstrates that the supine position in late pregnancy, causing aortic and venacaval compression, leads to brain auto-regulation that activates the brain sparing effect in the fetus. This protective mechanism, shown here for the first time to be linked to a physiological stress, may provide the basis for a novel approach in the assessment of fetal wellbeing.

Involvement of 5-HT2A receptors in genetic mechanisms of autoregulation of brain 5-HT system

The brain serotonin (5-HT) system has been implicated in the pathophysiology of anxiety, depression, drug addiction, and schizophrenia. 5-HT2A receptors are involved in the mechanisms of stressinduced psychopathology and impulsive behavior. In this work, we investigated the role of 5-HT2A receptors in the autoregulation of the brain 5-HT system. Chronic treatment with DOI, a 5-HT2A receptor agonist (1.0 mg/kg, i.p./14 days), produced a considerable decrease in the number of 5-HT2A receptor-mediated head twitches in AKR/J mice, indicating the desensitization of 5-HT2A receptors. Chronic DOI treatment did not affect the expression of the 5-HT2A receptor gene in the midbrain, hippocampus and frontal cortex. At the same time, an increase in the expression of the gene encoding a key enzyme of 5-HT synthesis, tryptophan hydroxylase-2 (TPH-2), accompanied with an increase in TPH-2 activity and 5-HT levels, and decreased expression of the serotonin transporter (5-HTT) gene were observed in the midbrain of DOI-treated mice. These results provide new evidence of receptor-gene cross-talk in the brain 5-HT system and implication 5-HT2A receptors in the autoregulation of the brain 5-HT system.

Reperfusion Injury after Autologous Cranioplasty in a Patient with Sinking Skin Flap Syndrome

The sinking skin flap syndrome is a rare complication after a large craniectomy. It consists of a sunken skin above the bone defect with neurological symptoms such as severe headache, mental changes, focal deficits, or seizures. In patient with sinking skin flap syndrome, cerebral blood flow and cerebral metabolism are decreased by sinking skin flap syndrome, and it may cause the deterioration of autoregulation of brain. We report a case of a patient with sinking skin flap syndrome who suffered from reperfusion injury after cranioplasty with review of pertinent literature.

Asymmetric posterior reversible encephalopathy syndrome in patient with hyperplastic anterior choroidal artery

We describe a case of asymmetric PRES due to the presence of hyperplastic anterior choroidal artery (AChA) in a man affected by sever hypertension. Posterior reversible encephalopathy syndrome (PRES) has become synonymous with a unique pattern of brain vasogenic edema and predominates in the parietal and occipital regions, accompanied by clinical neurological alterations. Sever hypertension is a risk factor that exceeds the limits of brain autoregulation, leading to breakthrough brain edema. In our knowledge this is the first case reported in literature, in which a similar vascular abnormality is linked to a PRES syndrome.

701: Maternal supine recumbency leads to brain auto-regulation in the fetus and elicit the brain sparing effect in low risk pregnancies

The brain sparing phenomena in the fetus is a protective mechanism aimed at maintaining sufficient blood flow towards the brain during chronic or acute fetal stress such as that caused by hypoxemia or utero-placental insufficiency. In this study we investigated whether the brain sparing effect can be also elicited by a physiological stress associated with maternal posture.