Normal Perfusion Pressure Breakthrough Research Articles

Abstract Number ‐ 121: Flow Diversion Jet: A Dangerous Mechanism in the Flow Diversion Treatment of Giant Intracranial Aneurysms

Introduction We present a patient with a giant vertebrobasilar system aneurysm. This case provides an in‐depth analysis of the pathologic mechanism resulting in catastrophic distal hemorrhage following stent deployment due to the shared effects of normal perfusion pressure breakthrough (NPPB) and the Windkessel phenomenon. The Windkessel phenomenon and NPPB occur before and after treatment of various vascular malformations, respectively. These phenomena are hypothesized to contribute to the loss of cerebrovascular autoregulation. High flow lesions and giant aneurysms reduce blood flow in downstream vessels, causing chronic distal vasodilation to protect against ischemia. Sudden restoration of normal pulsatile flow, following treatment, compromises the integrity of distal vessels leading to potential catastrophic intracerebral hemorrhage. Methods A retrospective review of the patient’s medical record was performed. Results A 60‐year‐old female initially presenting with pulsatile neck mass was found to have dolichoectasia of the right cervical internal carotid artery and two large, irregular, vertebrobasilar aneurysms. Managed conservatively for 10 years before developing gait ataxia, new imaging revealed growth of the now giant, more distal aneurysm. Flow diversion with partial coiling of the aneurysms was pursued. Following deployment, DynaCT demonstrated catastrophic thalamic and midbrain hemorrhage with intraventricular extension. A review of intra‐aneurysmal pressure measurements, angiography, MRI, and neuromonitoring data strongly suggests rupture of multiple deep perforators following the conversion to laminar flow when the flow diverting chain was finalized. This suggests giant aneurysms chronically depress the distal pulse pressure by acting as a Windkessel reservoir. Flow diversion bypasses the reservoir increasing pulse pressure distal to the aneurysm, exceeding autoregulatory capacity, leading to hemorrhage. Conclusions This is the first case in the literature to describe NPPB and the Windkessel phenomenon in the attempt to treat giant aneurysms with flow diversion. Flow diversion bypasses the reservoir, suddenly changing turbulent flow to laminar flow. The resultant dramatic rise in pulse pressure distal to the aneurysm can exceed the autoregulatory mechanisms of small distal vessels such as perforating branches. While demonstrating a poor outcome, awareness of these mechanisms and meticulous intra‐operative blood pressure management may reduce or prevent complications. Further modeling of flow dynamics both before and following treatment of these aneurysms may lead to altered guidelines in the temporality of treatment due to potential catastrophic sequelae.

Intra- and post-operative acute hemorrhagic complications of Onyx embolization of brain arteriovenous malformations: A single-center experience.

BackgroundThe intra- and post-operative acute (within 72 h) hemorrhagic complications of endovascular treatment (EVT) for a brain arteriovenous malformation (BAVM) are disastrous. Thus, further experiential summaries are required to fully understand them.Materials and methodsThis was a retrospective study of 25 patients with consecutive BAVM who were treated via EVT with Onyx embolization and suffered intra- and post-operative acute hemorrhage. The clinical and imaging data of the patients were recorded, analyzed, and discussed.ResultTwenty-five patients were aged 11–70 years (mean, 37.2 ± 16.1 years), of whom 12 were female (48%, 12/25). Of the 25 hemorrhagic complications, 17 (68%, 17/25) were intraoperative, and 8 (32%, 8/25) were post-operative and occurred between 1 and 12 h after EVT. Of 17 intraoperative hemorrhages, 13 (76.5%, 13/17) were due to high-pressure Onyx casting. Of eight post-operative hemorrhages, six (75%, 6/8) were attributed to normal perfusion pressure breakthrough. The degree of nidus Onyx embolization was more than 2/3 or complete in seven (87.5%, 7/8) BAVMs. Draining vein occlusion was observed in eight (32%, 8/25) of 25 BAVMs. After hemorrhage, conservative treatment was administered in 12 (48%, 12/25) cases, and surgical management was performed in other cases. There were eight cases of mortality; the remaining 17 patients had follow-up data. Among them, 15 patients had good outcomes, with Glasgow Outcome Scale scores of 5 and 4, accounting for 60% (15/25).ConclusionIn EVT for BAVMs, intra- and post-operative acute hemorrhagic complications are disastrous; only 60% of patients have a good outcome. Therefore, high-pressure Onyx casting or casting too much Onyx at one time to pursue a high degree of nidus embolization should be performed cautiously, and primary draining vein occlusion should be avoided. In short, EVT needs to be performed carefully.

Examination of the Risk of Normal Perfusion Pressure Breakthrough and Occlusive Hyperemia after Cerebral Arteriovenous Malformation (AVM) Resection Using Intraoperative Cerebral Angiography

Examination of the Risk of Normal Perfusion Pressure Breakthrough and Occlusive Hyperemia after Cerebral Arteriovenous Malformation (AVM) Resection Using Intraoperative Cerebral Angiography

Normalization of Peri-Arteriovenous Malformation Hemodynamics Prior to Direct Microsurgery: 2-Dimensional Operative Video.

Arteriovenous malformations (AVMs) are highly complex vascular lesions characterized by abnormal connections between arteries and an intervening nidus. Definitive and safe treatment of AVMs may require the combination of multiple treatment modalities to address the various complex features of the AVM.1 Endovascular embolization can be used as an adjuvant to surgery in order to control deep feeders, reduce flow, and address high-risk features such as aneurysms. In addition, by progressively reducing the AVM flow, staged embolization can lead to normalization of peri-AVM hemodynamics and therefore may decrease the risk of postresection hemorrhage.2,3 In this operative video, we present a case of a 41-yr-old female who presented with progressively worsening left-sided hemiparesis. Magnetic resonance imaging (MRI) and angiography revealed a complex right fronto-parietal AVM with significant associated edema, likely due to the vascular steal phenomenon. The area of edema, which included the motor cortex, was thought to be at high risk for postoperative hemorrhage from normal perfusion pressure breakthrough. We therefore decided to proceed with staged presurgical embolization to gradually normalize the perilesional hemodynamics, and therefore possibly reduce the risk of postoperative morbidity. The patient underwent 3 embolization sessions at 6-wk intervals. An MRI after the last embolization showed near-complete resolution of the fluid-attenuated inversion-recovery (FLAIR) signal around the AVM. Microsurgical resection was performed on the day after the last embolization. The patient tolerated the procedure well and was discharged at her neurological baseline with mild contralateral hemiparesis, which has continued to improve at follow-up. Postoperative angiography showed complete resection of the AVM. The patient consented to the procedure as shown in this operative video and gave informed written consent for use of her images in publication.

Decoding the Onset of Intraoperative Normal Pressure Perfusion Breakthrough with Near-Infrared Spectroscopy and Jugular Venous Oxygen Saturation Catheter in a Case of Arteriovenous Malformation Surgery

AbstractMultimodal monitoring can be a useful tool to design an appropriate anesthesia technique in the intraoperative period during the surgical excision of an intracerebral arteriovenous malformation (AVM). Intraoperatively, hyperperfusion syndrome can be attributed to causes like insufficient blood pressure control, occlusion of venous drainage before complete resection of arterial feeders, or inadequate hemostatic control of distended capillaries receiving arterial flow. We would like to highlight the potential role of near-infrared spectroscopy and jugular venous oxygen saturation catheter in detection of intraoperative normal perfusion pressure breakthrough and take necessary measures to prevent further insult with the help of this case report.

Neuroprotective effect of indomethacin in normal perfusion pressure breakthrough phenomenon

Loss of cerebral autoregulation in normal perfusion pressure breakthrough (NPPB) phenomenon has been reported in other Central Nervous System diseases such as neonatal intraventricular haemorrhage. Several studies have demonstrated that low-dose indomethacin prevents this latter condition. A previous rat model was used to resemble NPPB phenomenon. Study animals were distributed in 4 groups that received 3 doses of indomethacin at different concentrations prior to fistula occlusion 60 days after its creation. Control animals received saline solution. Intracranial pressure (ICP) increased in all groups following fistula creation, whereas mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) decreased as a manifestation of cerebral hypoperfusion and intracranial hypertension. The administration of indomethacin was associated with raised MAP and CPP, as well as decreased ICP. Sodium fluorescein extravasation was slight in study animals when comparing with control ones. Histological analysis evidenced diffuse ischaemic changes with signs of neuronal apoptosis in all brain layers in control animals. These findings were only focal and slight in study animals. The results suggest the usefulness of indomethacin to revert, at least partially, the haemodynamic effects of NPPB phenomenon in this experimental model, as well as to reduce BBB disruption and histological ischemia observed in absence of indomethacin.

Experimental rat model of chronic cerebral hypoperfusion–reperfusion mimicking normal perfusion pressure breakthrough phenomenon

BackgroundNormal perfusion pressure breakthrough (NPPB) phenomenon is a major life-threatening complication that restricts the treatment of complex intracranial arteriovenous malformations. The aim of the study it to develop a rat model mimicking NPPB phenomenon that enables the evaluation of any therapy to prevent such complication. MethodsTwenty Wistar male rats were randomly assigned to either a study or a control group. Study animals underwent an end-to-side left external jugular vein-common carotid artery anastomosis and ligation of bilateral external carotid arteries. Control animals only underwent ligation of bilateral external carotid arteries. All animals were sacrificed sixty days after the procedure. Hemodynamic parameters [mean arterial pressure (MAP), intracranial pressure (ICP) and cerebral perfusion pressure (CPP)], blood–brain barrier (BBB) permeability (measured by fluorescein staining) and histological features were then compared between both groups. ResultsA significant decrease in MAP and CPP was confirmed in the study group. An increase in ICP was also observed. A significant decrease in MAP and CPP was also present in the study group when comparing preoperative values with those recorded on days 0 (postoperative), 7 and 60. Fluorescein staining findings were consistent with signs of BBB disruption in study animals. Histological analysis demonstrated an increased number of pyknotic neurons in the ipsilateral hemisphere of rat brains included in the study group. ConclusionThese results confirm that this model mimics a vascular steal state with chronic cerebral hypoperfusion comparable to patients with AVMs behavior and disruption of the BBB after fistula closure comparable to NPPB phenomenon disorders.

Experimental rat model of chronic cerebral hypoperfusion-reperfusion mimicking normal perfusion pressure breakthrough phenomenon.

Normal perfusion pressure breakthrough (NPPB) phenomenon is a major life-threatening complication that restricts the treatment of complex intracranial arteriovenous malformations. The aim of the study it to develop a rat model mimicking NPPB phenomenon that enables the evaluation of any therapy to prevent such complication. Twenty Wistar male rats were randomly assigned to either a study or a control group. Study animals underwent an end-to-side left external jugular vein-common carotid artery anastomosis and ligation of bilateral external carotid arteries. Control animals only underwent ligation of bilateral external carotid arteries. All animals were sacrificed sixty days after the procedure. Hemodynamic parameters [mean arterial pressure (MAP), intracranial pressure (ICP) and cerebral perfusion pressure (CPP)], blood-brain barrier (BBB) permeability (measured by fluorescein staining) and histological features were then compared between both groups. A significant decrease in MAP and CPP was confirmed in the study group. An increase in ICP was also observed. A significant decrease in MAP and CPP was also present in the study group when comparing preoperative values with those recorded on days 0 (postoperative), 7 and 60. Fluorescein staining findings were consistent with signs of BBB disruption in study animals. Histological analysis demonstrated an increased number of pyknotic neurons in the ipsilateral hemisphere of rat brains included in the study group. These results confirm that this model mimics a vascular steal state with chronic cerebral hypoperfusion comparable to patients with AVMs behavior and disruption of the BBB after fistula closure comparable to NPPB phenomenon disorders.

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 postoperative 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 of a CCSDH.

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.

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).

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.

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.

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.

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.

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.