Normal Perfusion Pressure Research Articles

Postoperative management with dexmedetomidine in a pregnant patient who underwent AVM nidus removal: a case report

BackgroundFollowing cerebral arteriovenous malformation (AVM) surgery, severe brain edema and hemorrhage may be caused by postoperative normal perfusion pressure breakthrough (NPPB). Sedation is necessary for this population. It is a challenge for the anesthesiologist to maintain hemodynamic stability without interfering with the neurological assessment. In Japan, propofol is contraindicated for pregnant patients. Dexmedetomidine is a versatile drug in anesthesia practice and may be useful for this situation. There is no report using dexmedetomidine for the purpose of NPPB control in pregnant patients. We describe the postoperative management with dexmedetomidine for a pregnant patient who underwent cerebral AVM nidus removal.Case presentationA 32-year-old patient presented with headache at the 16th week of gestation. Neuroimaging revealed an intraventricular hemorrhage and an AVM at the right anterior horn of the lateral ventricle which caused bleeding. A multidisciplinary team discussion was done, and then a craniotomy for AVM nidus removal was performed under general anesthesia. Preanesthetic aspiration prophylaxis and rapid sequence induction were added to our conventional anesthetic management. Hypotension occurred after anesthetic induction but the patient recovered by volume resuscitation and vasopressors. Anesthesia was maintained with 50% O2 in air and sevoflurane. The AVM was completely removed, and no perioperative complications occurred. Postoperative sedation with dexmedetomidine was used to prevent breakthrough hyperperfusion and cerebral edema.ConclusionsDexmedetomidine infusion was used for postoperative sedation without causing any side effects, and it can be an alternative for sedation, especially when propofol is contraindicated.

Calcified chronic subdural hematoma: A case report and literature review

Calcified chronic subdural hematoma (CCSDH) is a rare disease that accounts for approximately 0.3%-2.7% of all chronic subdural hematomas (CSDHs). The clinical features of CCSDH are very similar to those of noncalcified CSDH and include headache, decreased alertness, weakness, numbness, gait disturbance, seizures, memory impairment, confusion, and unconsciousness. All symptomatic CCSDH should be treated surgically. Majority of these patients recover well following surgery. In this report, we present the case of a patient with CCSDH who developed severe cerebral edema following its removal, necessitating decompressive craniectomy. Although there were no abnormal findings in laboratory blood tests, and no signs of brain herniation or epilepsy was found the following day after surgery, the patient's family refused all treatment and a post-operative brain computed tomography (CT) scan. The patient was discharged and died at home. Cerebral hematoma and normal perfusion pressure breakthrough (NPPB) may cause severe cerebral edema following the total removal l of a CCSDH.

Ventricular-arterial coupling assessment using gated single-photon emission computed tomography: relationship with reserve pulse pressure and repolarization abnormalities.

In patients with normal myocardial perfusion, ST-segment depression and reserve pulse pressure (rPP) can identify patients at higher risk of cardiovascular events. We aimed to explore the prevalence of impaired ventricular-arterial coupling (VAc) in patients with normal myocardial perfusion imaging and its relationship with ST-segment depression and rPP. The present study included consecutive patients with normal myocardial perfusion imaging by single-photon emission computed tomography and ST-segment depression. Stroke volume, end-systolic pressure, arterial elastance (Ea), ventricular elastance (Ev), and VAc (Ea/Ev) were estimated both at rest and during stress. The difference between stress and rest (ΔVAc) was calculated. A positive ΔVAc was considered an impaired ΔVAc (iVAc). A total of 92 patients were prospectively included. iVAc was identified in 44 (59%) patients with ST-segment depression compared with 3 (16%) patients with normal repolarization (P=0.001). A higher incidence of abnormal rPP was identified in patients with ST-segment depression compared with the control group (61 vs. 16%, P=0.0001). ST-segment depression was identified as the only independent predictor of iVAc (adjusted OR 7.5; 95% CI 1.9-30.0, P=0.004). Noninvasive assessment of VAc is feasible with gated single-photon emission computed tomography and appears to be related to ST-segment depression and reserve rPP.

Spinal vascular malformations: treatment strategies and outcome.

Spinal vascular malformations (SVMs) are a heterogeneous group that can cause acute, subacute, or chronic spinal cord dysfunction. The majority of the patients present to neurosurgical attention after a protracted course with severe neurological dysfunction. Spinal vascular lesions comprise approximately 3-4% of all intradural spinal lesions. They are pathologically similar to their intracranial counterparts, but their clinical impact is often comparatively worse. Early, correct recognition of the pathology is mandatory to halt the progression of the disease and minimize permanent spinal cord injury. The first clinical observation of a SVM was published in 1890, but it was not until 1914 that the first successful surgical treatment of a spinal vascular malformation was reported. Intervention-either by microsurgical or endovascular means-aims to halt or reverse the progressive neurological deterioration by eliminating flow through the abnormal fistulous or nidal connections, and restoring normal spinal cord perfusion and intravascular pressures. In fact, complex spinal arteriovenous malformations (AVMs) and arteriovenous fistulas (AVFs) frequently require a multimodality approach that utilizes both microsurgery and endovascular embolization effectively. The goal of this review is to describe the various types of vascular malformations of the spine, their pathophysiology, clinical presentation, treatment strategies, and outcome. For purposes of discussion on the current manuscript, vascular malformations of the spine were divided into arteriovenous fistulas (AVFs) and arteriovenous malformations (AVMs). Spinal cord aneurysms are extremely rare, and the majority of the lesions that come to the neurosurgeon's attention are concomitant to a spinal AVM.

Combined Microneurosurgical and Endovascular Management of Grade V Occipital Arteriovenous Malformation: Sequential Delayed Embolization Holds the Key!

A 26-year-old previously healthy woman presented with complaints of sudden-onset headache, decreased level of consciousness, right hemiparesis, and hemianopia. Computed tomography (CT) of the head showed a leftsided parietal hematoma (►Fig. 1). CT angiography showed a complex arteriovenous malformation (AVM) with a venous varix in the center of the hematoma. Cerebral angiogram revealed a grade V AVM in the left parieto-occipital region measuring 6 4 cm and supplied by left posterior cerebral artery (PCA) and middle cerebral artery (MCA) and draining into superior sagittal sinus (SSS) and straight sinus via internal occipital vein/vein of Galen (►Fig. 2). Elective sequential endovascular embolization of the nidus was planned over 3 months in four settings. The aim of partial embolization over weeks was to occlude deep feeders and reduce the nidus to allow definitive treatment, either surgical resection or radiosurgery. Gradual flow reduction should also help prevent normal perfusion pressure breakthrough (NPPB) that might happen due to sudden hemodynamic changes during rapid occlusion of large, highflow AVMs. The treatment plan was developed in a way that each embolization would occlude less than 40% of the arterial feeders and nidus penetration would be limited. MCA feeders were embolized first, followed by the PCA feeders. Onyx (Covidien; Irvine, California, United States) was used in all sessions. It is composed of EVOH (ethylene vinyl alcohol) copolymer dissolved in DMSO (dimethyl sulfoxide), and suspended micronized tantalum powder to provide contrast for visualization under fluoroscopy. Standard technique was used with Apollo catheters with Mirage guidewires (Covidien; Irvine, California, United States) and Onyx 18 and 34 was injected into the nidus. The choice between 18 and 34 was based on flow characteristics observed during the superselective angiograms. At the end of last session of embolization, only small superficial cortical MCA and PCA feeders were left patent (►Fig. 3). The little flow lead to the decision to surgically excise the nidus. The patient underwent left-sided occipital craniotomy and excision of the nidus without complications (►Fig. 4). Postoperative angiogram showed complete resection (►Fig. 5).

Sepsis-Associated Coagulopathy: Diagnosis With Hematologic Biomarkers and a Novel Hemostatic Score That May Predict the Risk of Developing a Multiple Organ Dysfunction Syndrome and a Higher Rate of Mortality

SESSION TITLE: Sepsis and Shock Posters SESSION TYPE: Original Investigation Poster PRESENTED ON: Wednesday, October 28, 2015 at 01:30 PM - 02:30 PM PURPOSE: Severe Sepsis(SS)is associated with acute organ dysfunction. Different mechanisms are involved in the development of organ failures. Hemodynamic instability is the most important. Systemic inflammation, associated with SS, leads to production of pro-inflammatory cytokines. This can induce a procoagulant state:Activation of the Coagulation Cascade, Down-Regulation of Natural Anticoagulants, Inhibition of Endogenous Fibrinolysis. Fibrin formation and deposition, may produce thrombii in the microvasculature, disrupt blood flow to vital organs, and give rise to a Multiple Organ Dysfunction Syndrome(MODS). METHODS: Definition of DIC is based on a scoring system, that uses biomarkers:Platelets, PT, D-Dimers, Fibrinogen. We have changed it, by adding Protein-C(PC) and Antithrombin(AT), two Natural Anticoagulants, and deleting Fibrinogen, an acute phase reactant.74 patients, in the ICU with a diagnosis of sepsis, were screened for:All-cause mortality during hospital stay, Number of Organs showing an acute Dysfunction(NOD), Hematologic Biomarkers, Calculation of our Novel Hemostatic Score(HS)described in Dec.2012:CritCareMed. Suppl. Abstract:818, and Oct.2014:CHEST:146. Suppl. MeetingAbstracts:233A. RESULTS: All-cause mortality was 55%(41/74).The 41 patients who died had an average of 5.5NOD, while the 33 survivors had a mean NOD of 3.5(p<0.001).Patients who died showed an average HS of 8.8 points, compared to 6.6 in survivors(p=0.001).A significant difference in PC was noted between patients who died(0.34Un/l), compared with those who survived(0.53Un/l)(p<0.001).AT values were respectively 0.41Un/l and 0.55Un/l in patients who died, compared to survivors(p=0.003).Average Platelet counts were 101 in patients who died, and 154 in survivors(p=0.011). CONCLUSIONS: Our study showed a significant relationship between the severity of Sepsis-Associated Coagulopathy(SAC), and a worse clinical outcome. Low values of Natural Anticoagulants PC and AT, and a high HS, were all related with an increased NOD, and a higher rate of MODS and mortality. CLINICAL IMPLICATIONS: Restoring a normal perfusion pressure, may not be enough to prevent vital organs hypoxia, MODS, and death. DIC is now recognized as an independant predictor of mortality. Recombinant human Activated Protein-C(rhAPC), was withdrawn, because of poor results seen in PROWESS-SHOCK trial. But, Its main inclusion criterion was hemodynamic(septic shock), while rhAPC only has hematologic mechanisms of action. Past studies showed that patients who improved the most from getting rhAPC, were those with a SAC.New studies are needed. DISCLOSURE: The following authors have nothing to disclose: Jean Mathieu, Sylvie Boucher No Product/Research Disclosure Information

Normal perfusion pressure breakthrough theory: a reappraisal after 35 years.

The intrinsic ability of the brain to maintain constant cerebral blood flow (CBF) is known as cerebral pressure autoregulation. This ability protects the brain against cerebral ischemia and hyperemia within a certain range of blood pressures. The normal perfusion pressure breakthrough (NPPB) theory described by Spetzler in 1978 was adopted to explain the edema and hemorrhage that sometimes occur after resection of brain arteriovenous malformations (AVMs). The underlying pathophysiology of edema and hemorrhage after AVM resection still remains controversial. Over the last three decades, advances in neuroimaging, CBF, and cerebral perfusion pressure (CPP) measurement have both favored and contradicted the NBBP theory. At the same time, other theories have been proposed, including the occlusive hyperemia theory. We believe that both theories are related and complementary and that they both explain changes in hemodynamics after AVM resection. The purpose of this work is to review the current status of the NBBP theory 35 years after its original description.

Critical cerebral perfusion pressure at high intracranial pressure measured by induced cerebrovascular and intracranial pressure reactivity.

The lower limit of cerebral blood flow autoregulation is the critical cerebral perfusion pressure at which cerebral blood flow begins to fall. It is important that cerebral perfusion pressure be maintained above this level to ensure adequate cerebral blood flow, especially in patients with high intracranial pressure. However, the critical cerebral perfusion pressure of 50 mm Hg, obtained by decreasing mean arterial pressure, differs from the value of 30 mm Hg, obtained by increasing intracranial pressure, which we previously showed was due to microvascular shunt flow maintenance of a falsely high cerebral blood flow. The present study shows that the critical cerebral perfusion pressure, measured by increasing intracranial pressure to decrease cerebral perfusion pressure, is inaccurate but accurately determined by dopamine-induced dynamic intracranial pressure reactivity and cerebrovascular reactivity. Cerebral perfusion pressure was decreased either by increasing intracranial pressure or decreasing mean arterial pressure and the critical cerebral perfusion pressure by both methods compared. Cortical Doppler flux, intracranial pressure, and mean arterial pressure were monitored throughout the study. At each cerebral perfusion pressure, we measured microvascular RBC flow velocity, blood-brain barrier integrity (transcapillary dye extravasation), and tissue oxygenation (reduced nicotinamide adenine dinucleotide) in the cerebral cortex of rats using in vivo two-photon laser scanning microscopy. University laboratory. Male Sprague-Dawley rats. At each cerebral perfusion pressure, dopamine-induced arterial pressure transients (~10 mm Hg, ~45 s duration) were used to measure induced intracranial pressure reactivity (Δ intracranial pressure/Δ mean arterial pressure) and induced cerebrovascular reactivity (Δ cerebral blood flow/Δ mean arterial pressure). At a normal cerebral perfusion pressure of 70 mm Hg, 10 mm Hg mean arterial pressure pulses had no effect on intracranial pressure or cerebral blood flow (induced intracranial pressure reactivity = -0.03 ± 0.07 and induced cerebrovascular reactivity = -0.02 ± 0.09), reflecting intact autoregulation. Decreasing cerebral perfusion pressure to 50 mm Hg by increasing intracranial pressure increased induced intracranial pressure reactivity and induced cerebrovascular reactivity to 0.24 ± 0.09 and 0.31 ± 0.13, respectively, reflecting impaired autoregulation (p < 0.05). By static cerebral blood flow, the first significant decrease in cerebral blood flow occurred at a cerebral perfusion pressure of 30 mm Hg (0.71 ± 0.08, p < 0.05). Critical cerebral perfusion pressure of 50 mm Hg was accurately determined by induced intracranial pressure reactivity and induced cerebrovascular reactivity, whereas the static method failed.

Intraoperative Monitoring of Brain Tissue Oxygenation During Arteriovenous Malformation Resection

In normal perfusion pressure breakthrough (NPPB) it is assumed that following arteriovenous malformation (AVM) resection, vasoparalysis persists in the margins of the lesion and that a sudden increase in cerebral blood flow (CBF) after AVM exclusion leads to brain swelling and postsurgical complications. However, the pathophysiology NPPB remains controversial.The aim of our study was to investigate the oxygenation status in tissue surrounding AVMs and in the distant brain using intraoperative monitoring of cerebral partial pressure of oxygen (PtiO(2)) to achieve a better understanding of NPPB pathophysiology. Patients with supratentorial AVMs were monitored intraoperatively using 2 polarographic Clark-type electrodes. To establish reference values, we also studied PtiO(2) in a group of patients who underwent surgery to treat incidental aneurysms. Twenty-two patients with supratentorial AVMs and 16 patients with incidentally found aneurysms were included. Hypoxic pattern was defined as PtiO(2)≤15 mm Hg and/or PtiO(2)/PaO(2) ratio ≤0.10. Tissue hypoxia was detected in 63.6% of the catheters placed in the perinidal area and in 43.8% of catheters placed in a distant area. AVM excision significantly improved oxygenation both around the AVM and in the distant area. The PtiO(2)/PaO(2) ratio is a better indicator than absolute PtiO(2) in detecting tissue hypoxia in mechanically ventilated patients. Intraoperative monitoring showed tissue hypoxia in the margins of AVMs and in the distant ipsilateral brain as the most common finding. Surgical removal of AVMs induces a significant improvement in the oxygenation status in both areas.

Normal perfusion pressure breakthrough phenomenon: experimental models.

One of the most life-threatening complications after the obliteration of intracranial arteriovenous malformations is the development of oedema and/or multifocal haemorrhage. Two main theories have been postulated so far in order to explain this situation. On one hand, "normal perfusion pressure breakthrough phenomenon" is based on the loss of cerebral vessel autoregulation due to the chronic vasodilation of perinidal microcirculation. On the other hand, the "occlusive hyperaemia" deals with thrombotic and venous obstruction phenomena that may also generate such manifestations. The aim of this study is to resume the main concepts of the "normal perfusion pressure breakthrough phenomenon" theory as well as the related animal models described up to date, their advantages and disadvantages, and the main conclusions obtained as a result of the experimental research.

Importance of the Venous Outflow Pattern in Predicting Hyperemic Complications After Treatment of Cerebral Arteriovenous Malformations

odern treatment of cerebral arteriovenous malformations (AVMs) has evolved in the era of preoperative M embolization and radiosurgical treatment into a multidisciplinary, patient-specific approach that carefully balances the natural history of the disease with the inherent risks of surgical, endovascular, or radiosurgical treatments. Despite excellent results of AVM obliteration, the postoperative course of these patients can be complicated by hyperemic events, which can result in cerebral edema and intracerebral hemorrhages (3). Whether hyperemia occurs secondary to reperfusion of previously hypoperfused areas owing to poor arterial autoregulation (normal perfusion pressure breakthrough) or active hyperemia (2, 8) or secondary to occlusion of venous outflow (occlusive or passive hyperemia (1)), it has a significant impact on the morbidity and mortality of these patients. As previously shown by several studies, larger, more complex AVMs are associated with higher rates of hyperemic complications (7), but the pathophysiology of these events is unclear, and a predictive tool to identify patients with higher risks of hyperemic complications could modify postoperative care and improve patient outcomes.

Aortic Intussusception Complicating Diagnostic Angiography: Recognition and Management

During the diagnostic evaluation of a 31-year-old male with Marfan syndrome, an acute type B aortic dissection, and rising creatinine, the retrograde loop of our selective catheter inadvertently engaged the entry tear of the dissection in the mid-descending aorta. Traction on the catheter led to a full circumferential dehiscence of the remaining lumen, causing an intimointimal intussusception down to the level of the celiac artery with complete collapse of the true lumen and visceral and renal artery obstruction. Balloon fenestration and supramesenteric stenting of the true lumen decompressed the intussuscepted intimal flap and restored normal perfusion pressures.

Total resection in a giant left frontal arteriovenous malformation, grade V Spetzler-Martin - Case report

Abstract Background: Giant arteriovenous malformations (AVMs) are congenital lesions, with nidus sizing more than 6 cm. According to Spetzler-Martin scale, grade V AVMs have a nidus larger than 6 cm in diameter, profound venous drainage and are located in eloquent areas. Method: We report a case of a 39 years old woman, with giant left frontal AVM, grade V Spetzler-Martin, who was admitted for generalized seizures, with onset 32 years ago, refractory to full dose antiepileptic polytherapy, which severely impaired the patient’s quality of life. Results: The patient underwent surgery and we performed total resection of the AVM. We emphasize on surgical technique, intraoperative difficulties and outcome. Conclusions: Surgery is the therapy of choice in AVMs, because it provides cure of the lesion, and is the only treatment capable of preventing hemorrhage and controlling seizures. Management in grade V AVMs is challenging, because of their large size, multiple dilated arterial feeders from anterior and posterior circulation and external carotid arteries, high blood flow, vascular steel from the surrounding brain, enlarged draining veins, profound venous drainage and location in eloquent area. Giant AVMs with high flow nidus, causing a great degree of vascular steel in the surrounding brain, with hypoperfusion of normal parenchyma may develop early normal perfusion pressure breakthrough. Total resection in grade V AVMs can be performed with minimal transient morbidity and favorable outcome. Total resection permits control of intractable seizures with reduced dose of antiepileptic therapy.

The evaluation of cerebral function by diffusion weighted imaging after norepinephrine-induced hypertensive perfusion therapy in pig model of cardiac arrest

To evaluate the changes in cerebral function of pigs with cardiac arrest (CA) after recovery of spontaneous circulation (ROSC) after hypertension perfusion therapy induced by norepinephrine (NE). Ventricular fibrillation (VF) was induced by electrical stimulation, and standard cardiopulmonary resuscitation (CPR) was performed after VF for 4 minutes. The pigs with successful ROSC were randomly divided into two group, each n=5. The pigs in the hypertensive reperfusion group were given with NE immediately to maintain the mean arterial pressure (MAP) at 130% before VF for 4 hours; MAP of the pigs in normal reperfusion group was maintained for 4 hours as baseline. The changes in hemodynamics were observed for 4 hours in both groups. Cerebral cortex was scanned with diffusion weighted imaging (DWI) before VF and 1 hour and 3 hours after ROSC, and the dynamic changes in brain functional imaging were observed. Twenty-four hours after ROSC, brain biopsy were collected and examined after hematoxylin and eosin staining (HE). Compared with the normal reperfusion group, heart rate (HR), MAP, cardiac output (CO) and coronary perfusion pressure (CPP) in the hypertensive reperfusion group showed a tendency to increase (ROSC 30 minutes HR: 167±8 bpm vs. 140±15 bpm, ROSC 1 hour MAP: 131±9 mm Hg vs. 108±10 mm Hg, ROSC 1 hour CO: 4.9±0.1 L/min vs. 3.4±0.5 L/min, ROSC 2 hours CPP: 118±12 mm Hg vs. 88±1 mm Hg, P<0.05 or P<0.01). There was no obvious abnormality as shown by DWI before and after resuscitation, and the apparent diffusion coefficient (ADC) showed a tendency to decrease after resuscitation in both groups. The ADC in the normal reperfusion group was decreased more than that in the hypertensive reperfusion. Pathological study showed that the protective effect of the hypertensive reperfusion on brain tissue was better than that of the normal reperfusion group. Hypertensive reperfusion can produce hemodynamic changes, and an increase in cerebral blood flow, thus it produces a protective effect on brain to promote the recovery of neurological function in pigs with CA after resuscitation.

Normal Perfusion Pressure Breakthrough Following AVM Resection: A Case Report and Review of the Literature

Objective: To report a patient’s clinical course illustrative of the NPPB mechanism for hyperperfusion-induced injury. Methods: A 65-year-old female presented with a severe headache and was found to have a 6-cm right parietal AVM on imaging. The patient underwent staged, pre-operative embolization and the AVM was surgically resected without intra-operative complication. After the patient emerged from anesthesia she exhibited left hemiplegia and hemispatial neglect. Her systolic blood pressure (SBP) at that time was between 110-120 mmHg. SBP was reduced to 90-100 mmHg and the patient’s symptoms resolved shortly thereafter. The patient’s strict blood pressure goal was relaxed the next morning. However, with her SBP 110-120 mmHg in the ensuing hours, the patient’s left-sided neglect and hemiparesis returned. Her SBP was reduced again to 90-100 mmHg, leading to resolution of her symptoms. Results: This patient’s clinical course supports the NPPB theory of hyperperfusion-induced injury. Despite CT imaging demonstrating no residual AVM following resection, the patient developed neurological deficits in the immediate postoperative period. Aggressive systemic hypotension improved clinical symptoms repeatedly, whereas a brief period of normotension triggered a return of neurological deficits. As a result, there was a direct correlation between fluctuations of neurological status and SBP. This case suggests that the intrinsic autoregulatory capacity was altered in our patient, and that aggressive hypotension was necessary to compensate for diminished autonomic reactivity. Conclusions: This case provides further evidence that NPPB plays a role in hyperperfusion-induced injury following AVM excision and that blood pressure control is vital in managing hyperemic complications following complete resection of cerebral AVMs.

Microneurosurgery in combination with endovascular embolisation in the treatment of solid haemangioblastoma in the dorsal medulla oblongata

ObjectiveTo investigate the treatment of solid haemangioblastomas in the dorsal medulla oblongata using microneurosurgery in combination with endovascular embolisation. MethodsClinical data from 11 patients with solid haemangioblastomas in the dorsal medulla oblongata who were treated with endovascular embolisation followed by microneurosurgery were analysed retrospectively. Clinical results were evaluated using the modified Rankin scale. The patients were preoperatively evaluated by neuroimaging methods such as magnetic resonance imaging (MRI), contrast MRI and digital subtraction angiography (DSA). General anaesthesia was induced, the patients were tracheally intubated, and the abnormal vessels were embolised. Surgery to resect the haemangioblastoma was conducted after the blood-clotting index returned to normal levels (generally one month after the interventional treatment). ResultsEmbolisation was accomplished in all 11 patients. DSA analysis revealed that most of the tumour vessels and tumour stains disappeared without any complications. The haemangioblastomas were completely resected. None of the patients received blood transfusion or died during surgery. The neurological deficit was reduced or eliminated in 10 patients, but 1 patient died after experiencing an acute myocardial infarction on the tenth postoperative day. No recurrence occurred during follow-up in patients who underwent total tumour resection. Postoperative grades using the modified Rankin scale were improved in all 10 patients. However, several complications occurred, including communicating hydrocephalus, incision infection, pneumonia and cerebrospinal fluid leakage from the incision. Notably, normal perfusion pressure breakthrough (NPPB) did not develop during or after endovascular embolisation or surgery. ConclusionPreoperative endovascular embolisation is a safe and effective adjunct treatment. Employing this treatment, solid haemangioblastomas in the dorsal medulla oblongata can be safely and completely resected.

Intracoronary glucagon-like peptide 1 preferentially augments glucose uptake in ischemic myocardium independent of changes in coronary flow

We examined the acute dose-dependent effects of intracoronary glucagon-like peptide (GLP)-1 (7-36) on coronary vascular tone, cardiac contractile function and metabolism in normal and ischemic myocardium. Experiments were conducted in open chest, anesthetized dogs at coronary perfusion pressures (CPP) of 100 and 40 mmHg before and during intracoronary GLP-1 (7-36) infusion (10 pmol/L to 1 nmol/L). Isometric tension studies were also conducted in isolated coronary arteries. Cardiac and coronary expression of GLP-1 receptors (GLP-1R) was assessed by Western blot and immunohistochemical analysis. GLP-1R was present in the myocardium and the coronary vasculature. The tension of intact and endothelium-denuded coronary artery rings was unaffected by GLP-1. At normal perfusion pressure (100 mmHg), intracoronary GLP-1 (7-36) (targeting plasma concentration 10 pmol/L to 1 nmol/L) did not affect blood pressure, coronary blood flow or myocardial oxygen consumption (MVO(2)); however, there were modest reductions in cardiac output and stroke volume. In untreated control hearts, reducing CPP to 40 mmHg produced marked reductions in coronary blood flow (0.50 ± 0.10 to 0.17 ± 0.03 mL/min/g; P < 0.001) and MVO(2) (27 ± 2.3 to 15 ± 2.7 μL O(2)/min/g; P < 0.001). At CPP = 40 mmHg, GLP-1 had no effect on coronary blood flow, MVO(2) or regional shortening, but dose-dependently increased myocardial glucose uptake from 0.11 ± 0.02 μmol/min/g at baseline to 0.17 ± 0.04 μmol/min/g at 1 nmol/L GLP-1 (P < 0.001). These data indicate that acute, intracoronary administration of GLP-1 (7-36) preferentially augments glucose metabolism in ischemic myocardium, independent of effects on cardiac contractile function or coronary blood flow.

The effect of ventricular assist devices on cerebral blood flow and blood pressure fractality

Biological signals often exhibit self-similar or fractal scaling characteristics which may reflect intrinsic adaptability to their underlying physiological system. This study analysed fractal dynamics of cerebral blood flow in patients supported with ventricular assist devices (VAD) to ascertain if sustained modifications of blood pressure waveform affect cerebral blood flow fractality. Simultaneous recordings of arterial blood pressure and cerebral blood flow velocity using transcranial Doppler were obtained from five cardiogenic shock patients supported by VAD, five matched control patients and five healthy subjects. Computation of a fractal scaling exponent (α) at the low-frequency time scale by detrended fluctuation analysis showed that cerebral blood flow velocity exhibited 1/f fractal scaling in both patient groups (α = 0.95 ± 0.09 and 0.97 ± 0.12, respectively) as well as in the healthy subjects (α = 0.86 ± 0.07). In contrast, fluctuation in blood pressure was similar to non-fractal white noise in both patient groups (α = 0.53 ± 0.11 and 0.52 ± 0.09, respectively) but exhibited 1/f scaling in the healthy subjects (α = 0.87 ± 0.04, P < 0.05 compared with the patient groups). The preservation of fractality in cerebral blood flow of VAD patients suggests that normal cardiac pulsation and central perfusion pressure changes are not the integral sources of cerebral blood flow fractality and that intrinsic vascular properties such as cerebral autoregulation may be involved. However, there is a clear difference in the fractal scaling properties of arterial blood pressure between the cardiogenic shock patients and the healthy subjects.

Surgical treatment of giant intracranial arteriovenous malformations

To review surgical outcomes in treating intracranial Giant arteriovenous malformations (AVMs). To find out the prognosis factors of surgical treatment. We collected 46 consecutive cases of giant AVMs treated at Beijing Tiantan Hospital, reviewed the radiological and Spetzler-Martin grading. 25 of the patients selected were male (54%), and 21 were female (46%), with a mean age of 30.6. The major presenting symptoms were seizures, headaches, hemorrhage and neurological deficits. According to the Spetzler-Martin Grading, 8 patients were Grade III, 22 were Grade IV, and 16 were Grade V. All patients received surgical treatment and postoperative DSA were performed. Clinical results and long term follow-up (KPS) were gathered for analysis. One of the 35 patients who received postoperative DSA revealed residual AVMs. Among all patients, severe complications were observed in 9 patients, and 1 patient died in the hospital. Complications included hemiparalysis (15 cases), aphasia (6 cases), hemianopia (9 cases), cranial nerve dysfunction (5 cases), and seizure (5 cases). Normal perfusion pressure breakthrough (NPPB) was observed in 6 patients. After 6 - 108 months of follow-up, 33 of 37 survived follow-up patients presented normal function or minimal symptoms and ability to work or study, 4 patients died (2 were surgical-related). Pre-surgical evaluation of every candidates and treatment choice are the determining factors in giant AVMs therapy. Microsurgery remains one of the most effective ways for eliminating giant cerebral AVMs, and the complication rate was acceptable. For giant cerebral AVMs located superficially or do not involve critical components, a good outcome can be expected through surgical resection.

Revisiting normal perfusion pressure breakthrough in light of hemorrhage-induced vasospasm

Cerebral arteriovenous malformations (AVMs) have abnormally enlarged arteries and veins prone to spontaneous hemorrhage. Immediately following surgical excision of a cerebral AVM, even normal brain tissue surrounding the lesion is subject to hemorrhage, a phenomenon termed normal perfusion pressure breakthrough (NPPB) syndrome. According to this theory, arteries supplying cerebral AVMs become dilated and lose their capacity to dilate or constrict to autoregulate pressure. Acutely after removal of a cerebral AVM, excessive blood pressure in these arterial feeders can cause normal brain tissue to bleed. However, this theory remains controversial. We present a patient with a cerebral AVM that demonstrated cerebrovascular reactivity and argues against an assumption underlying the theory of NPPB syndrome.