Cerebral Arterial Spasm Research Articles

Results of assessing cerebral vasospasm following subarachnoid hemorrhage using transcranial doppler ultrasound

SUMMARY Objective: Review the results of assessing cerebral vasospasm after subarachnoid hemorrhage using transcranial doppler ultrasound. Subjects and methods: A retrospective, cross-sectional descriptive study was performed on 39 patients with subarachnoid hemorrhage treated at the Neurology Center, Bach Mai Hospital from January 2020 to September 2023. Results: The mean age of the study group was 55.12 ± 14.33. The age group distribution with the highest incidence is 41-50 years old with a rate of 35.9%. The male/female ratio is 20/19. The most common symptoms were headache (97.4%), nausea and vomiting (92.3%), The least common symptoms were convulsions and hemiplegia in 5.1% of subjects. The most common clinical severity assessed by the Hunt and Hess scale is level 2 (59%), followed by level 3 (23.1%), level 4 (10.2%), and level 1 (5.1%). Evaluation of Fisher scale found that the most common fisher level is level 4 with a rate of 33.6%, followed by level 3 (28.2%), level 1 (25.6%), the least common is grade 2 with 2.6%. The results of the second transcranial Doppler ultrasound performed on the sixth to eighth day of the disease is the time with the highest rate of vasospasm, showing the most vasospasm cerebral artery is the middle cerebral artery: right middle cerebral artery. 35.9%, left middle cerebral artery 12.8%. Next is anterior cerebral artery spasm: right anterior cerebral artery 23.1%, left anterior cerebral artery 2.6%. Right posterior cerebral artery 10.3%, left posterior cerebral artery 5.1%. Compared to the gold standard for diagnosing vasospasm, which is 128-slices MSCT, transcranial Doppler ultrasound has a sensitivity of 0.91, a specificity of 0.88, a positive predictive value of 0.91, and a negative predictive value of 0.88. The appropriateness of transcranial Doppler ultrasound and 128-slices computed tomography scan in diagnosing cerebral vasospasm after subarachnoid hemorrhage is very high, Kappa coefficient = 0.791, statistically significant with p < 0.05. Conclusion: Clinical symptoms of the disease are very diverse and non-specific, the most common symptom being headache is 97.4%. The most common Hunt and Hess scale to assess clinical severity is 2, however the most common Fisher scale is 4. Middle cerebral artery thrombosis has the highest rate of spasm, followed by the anterior cerebral artery. Compared to the gold standard for diagnosing vasospasm, which is 128-slices MSCT, transcranial Doppler ultrasound has a sensitivity of 0.91, a specificity of 0.88, a positive predictive value of 0.91, and a negative predictive value of 0.88

Hyperbaric Oxygen Mediated PI3K/Akt/mTOR Pathway in Inhibiting Delayed Cerebral Vasospasm after Subarachnoid Hemorrhage.

Delayed cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH) is a serious complication. This article aimed to explore the mechanism of hyperbaric oxygenation (HBO) inhibiting delayed CVS after SAH. The 60 SD rats were grouped: normal control group (NC), sham operation group (Sham), SAH Model (Model), and HBO treatment group. The SAH model was established by injecting blood twice into the cisterna magna (CM), and the neurological function of the rats were evaluated by modified Garcia scale. The plasma of the rats was collected at 1, 3, 6, and 9 days after HBO treatment. Plasma levels of PI3K/Akt/mTOR pathway-related proteins were detected by Western blot (WB). TUNEL method was used to observe the apoptosis rate of basilar artery (BA) endothelial cells (ECs). Hematoxylin-eosin staining (HE) staining was used to observe the inner diameter and the thickness of vessel wall of rat cerebral arteries. The relationship between mTOR and middle cerebral artery spasm was analyzed. As against the Model, the neurological function was visibly increased, the expressions of Bcl-2, PI3K, mTOR, and p-Akt/Akt protein in plasma were visibly increased, the expression of Bax protein was visibly decreased, and the degree of CVS was visibly reduced in the HBO group (all P < 0.05). The level of mTOR is negatively correlated with the degree of CVS after SAH, and HBO can inhibit the occurrence of delayed CVS.

Neuroanesthesia Management in Cavernous Sinus Meningioma Craniotomy Patients

The most prevalent primary cavernous sinus (CS) lesion is cavernous sinus meningioma (CSM). Of all intracranial neoplasms, 1% are tumors in CS, and 41% are CSM. For contemporary neurosurgeons, orbital involvement in cavernous sinus meningiomas (CSMs) poses special difficulties. The condition is known as cavernous sinus meningioma (CSM) gradually impairs vision and may ultimately result in chiastic compression. Since January 2023, a male 55-year-old had been admitted to the hospital with cephalgia and mild diplopia in his right eye. Cavernous meningiomas were discovered using CT scans, and a craniotomy procedure was scheduled to remove the tumor. In order to facilitate intubation, the patient was given a premedication of sufentanyl for analgesia and was then given general anesthesia. Rocuronium was used to relax the muscles. Desflurane is an attractive option available to anesthesiologists to maintain general anaesthesia. This surgical procedure of removing intracranial tumours requires proper induction and monitoring of the patient's condition during surgery to prevent increased intracranial pressure. Intracranial elevation can cause systemic changes such as hypertension and changes in heart rhythm, as well as cerebral artery spasm, and lead to cerebral infarction and cerebral ischemia. An effective neuroanesthesia management program can help preserve hemodynamic stability and improve results during craniotomy surgery for the removal of meningiomas

Association of endothelial nitric oxide synthase (Glu298Asp) gene polymorphism with radial artery spasm during cardiac catheterization in Egyptians

BackgroundNitric oxide (NO) exerts diverse effects on the cardiovascular system. Impairment of NO production plays a key role in cerebral and coronary artery spasm. We aimed to explore the predicting factors of radial artery spasm (RAS) and the association of eNOS gene polymorphism (Glu298Asp) with RAS during cardiac catheterization.Methods and results200 patients underwent elective coronary angiography through a trans-radial approach. The subjects were genotyped to the Glu298Asp polymorphism (rs1799983) on the eNOS gene by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Our results showed that the subjects with the TT genotype and T allele were significantly more likely to develop radial artery spasms (OR = 12.5, 4.6, P < 0.001 respectively). TT genotype of eNOS Glu298Asp polymorphism, number of punctures, size of the radial sheath, radial tortuosity, and right radial access are independent predictors of radial spasm.ConclusionThe eNOS (Glu298Asp) gene polymorphism is associated with RAS during cardiac catheterization in Egyptians. TT genotype of eNOS Glu298Asp polymorphism, number of punctures, size of the radial sheath, right radial access, and tortuosity are independent predictors of RAS during cardiac catheterization.

Carvedilol Reduces the Neuronal Apoptosis after Ischemic Stroke by Modulating Activator of Transcription 3 Expression in vitro

Cerebral ischemia is divided into local cerebral ischemia and diffuse cerebral ischemia. The etiology of localized cerebral ischemia includes middle cerebral artery embolism; stenosis, occlusion, or thrombosis of extracranial internal carotid artery or vertebral artery; and cerebral artery spasm. The causes of diffuse cerebral ischemia include cardiac arrest, hypotension, anemia, and hypoglycemia. However, the underlying mechanism is still unclear. In this study, we demonstrated that activator of transcription 3 (ATF3) is a hubgene in IS by bioinformatics analysis. The expression of ATF3 was increased in PC12 cells with oxygen-glucose deprivation/reoxygenation (OGD/R) treatment. ATF3 deficiency inhibited cell viability and induced cell apoptosis, whereas ATF3 overexpression showed the opposite role in cell viability and cell apoptosis. Moreover, Carvedilol as a compound targeting ATF3 also facilitated cell viability and reduced cell apoptosis. ATF3 deficiency retarded the increase in cell viability and inhibition of cell apoptosis in OGD/R-PC12 cells with Carvedilol treatment. Additionally, the decreased Bax and cleaved caspase-3 were released in OGD/R-PC12 cells with Carvedilol and siATF3 treatment, while Bcl-2 expression was inhibited in OGD/R-PC12 cells with Carvedilol and siATF3 treatment. In conclusion, Carvedilol may be a key compound targeting ATF3 in OGD/R-PC12 cells. Graphical : Carvedilol positively regulated cell viability and negatively regulated cell apoptosis in OGD/R-PC12 cells by inhibition of ATF3.

Acute and Delayed Cerebrovascular Injury From Gunshot to the Head in a 12-Year-Old Child During the COVID-19 Pandemic

Acute and Delayed Cerebrovascular Injury From Gunshot to the Head in a 12-Year-Old Child During the COVID-19 Pandemic

In Reply to the Letter to the Editor Regarding ‘Transtentorial Brain Herniation After Lumbar Drainage in Patient Planned for Cranioplastic Reconstruction: Catastrophic Play Between Atmospheric and Intracranial Pressure’

Cerebral vasospasm and delayed ischemic neurologic deficits are well-known clinical aftereffects of subarachnoid hemorrhage due to rupture of an intracranial aneurysm. However, vasospasm with consequential ischemia after clipping of an unruptured aneurysm is an exceedingly rare sequela encountered in the reported neurosurgical literature.A 53-year-old woman had presented for elective craniotomy with microsurgical clipping of an unruptured left middle cerebral artery bifurcation saccular aneurysm, which was successfully treated without complications. Despite an initially benign clinical course, she experienced diffuse vasospasm with profound ischemic neurologic deficits on postoperative day 13 with a left middle cerebral artery distribution ischemic infarct. Moreover, she developed recurrent delayed spasm of the right posterior cerebral artery on postoperative day 26 and, consequentially, a left homonymous hemianopsia despite treatment with intra-arterial verapamil infusion.To the best of our knowledge, we have reported the first case of recurrent cerebral vasospasm and delayed ischemia neurologic deficits weeks subsequent to clipping of an unruptured aneurysm. The findings from the present case highlight the importance of considering delayed vasospasm as a cause of acute onset neurologic symptoms for patients who have recently undergone elective aneurysm surgery. We also reviewed the current data regarding the epidemiology, surgical factors, and proposed pathophysiologic mechanisms related to vasospasm after elective cases.

Lower limb weakness with gyrus rectus hematoma: an unusual presentation of paraclinoid aneurysm; a case report with review of literature

Lower limb weakness is usually a feature of ruptured anterior communicating (ACom) aneurysms due to spasm of the anterior cerebral arteries. Paraclinoid aneurysms, in addition to other cardinal features of subarachnoid haemorrhage (SAH), usually present with headache and visual field defects due to compression of the optic pathway. We report a case of left paraclinoid aneurysm presenting with right lower limb weakness and gyrus rectus hematoma without SAH. The aneurysm was long, passing beneath the optic nerve to emerge in the inter-optic cistern, leading to such atypical presentation. The aneurysm was clipped successfully after drilling the clinoid. As per our knowledge, such a clinical presentation of paraclinoid aneurysm has not been reported in the literature till date.

Hyperbaric oxygen on rehabilitation of brain tumors after surgery and effects on TNF-α and IL-6 levels.

Hyperbaric oxygenation (HBO) on postoperative rehabilitation of brain tumors and effects on tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels were explored. A retrospective analysis of 132 patients with brain tumors treated in the People's Hospital of Rizhao from October 2014 to October 2017 was performed. There were 62 patients in the observation group and 70 patients in the control group. Patients in the control group were treated with conventional drugs, and patients in the observation group were treated with HBO on the basis of conventional drug therapy. Levels of serum TNF-α and IL-6 were measured by ELISA before and after treatment. Cerebral arterial flow velocity and spasticity were measured by cranial color Doppler ultrasonography. Neurological function deficit (NFD) and activities of daily living (ADL) were used to evaluate the clinical recovery of the patients. Clinical efficacy was compared and analyzed. There were no significant differences between the two groups before treatment (P>0.05). After treatment, serum TNF-α and IL-6 levels were significantly lower than pretreatment levels (P<0.05), and serum TNF-α and IL-6 levels in the observation group were lower than those in the control group (P<0.05). Cerebral arterial flow velocity in observation group after treatment was significantly lower than that in the control group. The number of patients with cerebral arterial spasm after treatment in the observation group was significantly smaller than that in the control group. NFD scores in the observation group were lower than those in the control group after treatment. After treatment, ADL scores in the observation group were significantly higher than those in the control group (P<0.05). The comprehensive treatment effect of HBO is significant. It can inhibit the expression of inflammatory factors in serum and reduce cerebral arterial flow velocity and effectively reduce the number of patients with cerebral arterial spasm. It can reduce NFD and improve the quality of life of patients. Therefore, it is worthy of clinical popularization.

Myogenic Trigger Zone of Trapezius Muscle Increases the Tone of the Middle Cerebral Artery

A myogenic trigger zone (MTZ) has been shown to affect the tone of the surface arteries of the head and lower limbs. However, it remains largely unknown whether the tone of the intracranial arteries is regulated by MTZ. The aim of the present study was to investigate the effect of MTZ in trapezius muscle on the tone of the middle cerebral artery. Using ultrasound measurements of the peak velocity of blood flow and the Lindegaard index (LI), we found that the presence of an active MTZ in a trapezius muscle was per se associated with an increased LI values and that pressure stimulation of the MTZ further increases LI. When MTZ was eliminated by means of manual therapy, the indices of blood flow and LI returned to normal values. We conclude that the reflex spasm of the middle cerebral artery can occur in the presence of an active MTZ-TM and that this phenomenon contributes to the pathogenesis and the clinical symptoms associated with the cervicogenic and tension headaches.

P13.13 * INTRAOPERATIVE RADIOTHERAPY WITH INTRABEAM IN PRIMARY BRAIN TUMORS AFTER RESECTION: PRELIMINARY REPORTS OF 26 CASES

OBJECTIVES: To evaluate the preliminary results of intraoperative radiotherapy (IORT) with Intrabeam (Zeiss) in patients with primary brain tumors. METHODS AND MATERIALS: Primary brain tumor patients were selected and treated with Intrabeam IORT to the tumor beds in our center after resection, the doses range from 8-12Gy with depth of 2mm from applicator surface. All patients were evaluated in serials CT/MRI scans and neurological function, blood cell counting and wound healing duration. RESULTS: Up-to-now, 26 cases of adult patients (age from 8-75) with malignant brain tumor were treated with IORT, which included 1 recurrent medulloblastoma, 3 recurrent glioblastoma,1 recurrent astrocytoma, 5 anaplastic mixed glioma, 2 astrocytoma (grade 2) and 12 new diagnosis glioblastoma, 2 epydenoma . 3 of them had been previously irradiated. Follow-up was 1month to 15 months. Until now, 6 patients died (2 died within 1 month after surgery, 4 died of recurrent tumors). Other 20 patients are still alive without tumor recurrence (1-14 month), follow-up MRI /CT scans did not show significant necrosis after IORT; 1 patients had bleeding in the tumor cavity (thalamus, died 20days later), 1 patient have paralysis 1 day after operation and recovered 10 days later because of cerebral artery spasm, others are all recovered totally from surgery without any complications, blood counting and wound healing duration were the same as no-IORT patients. No other toxicity was observed at the last follow-up visit. CONCLUSION: Our preliminary results of 26 cases during 1-15 months follow- up demonstrated that Intrabeam IORT to a dose of 8-12 Gy to 2 mm in the treatment of primary brain tumors beds are safe without increase post-operative complications, but long term follow up for recurrent malignant brain tumors were not satisfy, but for new diagnosis brain tumor patients showed good local tumor control with relatively long term survival. Further researches are needed to evaluate long term efficacy, especially for ependymomas and low grade glioma.

Etioloy and potential mechanism of cerebral infarction post severe traumatic brain injury

Objective To investigate the clinical characteristics,risk factors and potential mechanism of cerebral infarction post severe traumatic brain injury(TBI).Method Clinical records of 24 patients suffering cerebral infarction and 46 patients without cerebral infarction after severe TBI were reviewed retrospectively.Results patients with cerebral infarction got a survival rate at 58％,lower than patients without cerebral infarction (83％).The maximal body temperature (38.1 ± 0.8) ℃ in the first 24hrs,incidence of coagulating dysfunction (75％) and middle cerebral artery spasm(75％) were much higher in infarction group than the non-infarction group (P ＜ 0.05).Conclusion Cerebral infarction exerts a tremendous influence on the prognosis of severe TBI.Cerebral vessel spasm,devastation and compression of the vessel structure are the high risk factors for cerebral infarction after severe TBI. Key words: Brain trauma; Brain infarction; Cerebral vasospasm; High risk factors

Cannabis use: signal of increasing risk of serious cardiovascular disorders.

BackgroundCannabis is known to be associated with neuropsychiatric problems, but less is known about complications affecting other specified body systems. We report and analyze 35 recent remarkable cardiovascular complications following cannabis use.Methods and ResultsIn France, serious cases of abuse and dependence in response to the use of psychoactive substances must be reported to the national system of the French Addictovigilance Network. We identified all spontaneous reports of cardiovascular complications related to cannabis use collected by the French Addictovigilance Network from 2006 to 2010. We described the clinical characteristics of these cases and their evolution: 1.8% of all cannabis‐related reports (35/1979) were cardiovascular complications, with patients being mostly men (85.7%) and of an average age of 34.3 years. There were 22 cardiac complications (20 acute coronary syndromes), 10 peripheral complications (lower limb or juvenile arteriopathies and Buerger‐like diseases), and 3 cerebral complications (acute cerebral angiopathy, transient cortical blindness, and spasm of cerebral artery). In 9 cases, the event led to patient death.ConclusionsIncreased reporting of cardiovascular complications related to cannabis and their extreme seriousness (with a death rate of 25.6%) indicate cannabis as a possible risk factor for cardiovascular disease in young adults, in line with previous findings. Given that cannabis is perceived to be harmless by the general public and that legalization of its use is debated, data concerning its danger must be widely disseminated. Practitioners should be aware that cannabis may be a potential triggering factor for cardiovascular complications in young people.

Anaphylactic Shock Decreases Cerebral Blood Flow More Than What Would Be Expected From Severe Arterial Hypotension

To the Editor In a recent issue of Shock (1), a very important paper was published with the title: “Anaphylactic Shock Decreases Cerebral Blood Flow More Than What Would Be Expected From Severe Arterial Hypotension.” The authors of this article concluded that, in anaphylactic shock, severe impairment of the cerebral blood flow takes place, which could not be explained by the level of arterial hypotension. In their experiments with rat model of anaphylaxis, the tissue oxygen partial pressure decreased very rapidly, as early as 1 min following the onset of anaphylaxis, and this was attributed to the early and direct action of anaphylactic mediators on cerebral vessels. Indeed, mast cell mediators such as histamine, chymase, and leukotrienes can induce cerebral artery spasm (2), and platelet-activating factor can reduce cerebral blood flow (3), leading to postischemic hypoperfusion. Therefore, cerebral ischemia and brain injury following anaphylactic shock could be due to direct action of anaphylactic mediators on the cerebral arterial system and not due to arterial hypotension. The above came to support our view on pathophysiology of anaphylactic shock that systemic vasodilatation and plasma and volume loss due to vascular permeability, reduced venous return, reduced cardiac output, and coronary hypoperfusion are not the sole primary cause of tissue damage. Experimental and clinical evidence has shown that, in anaphylactic shock, the coronary arteries could be the primary target of anaphylaxis (4), resulting in the development of Kounis anaphylaxis–associated coronary syndrome (5). In an experiment with ovalbumin-sensitized guinea pigs, which took place more than 20 years ago (6), it was concluded that the registered anaphylactic damage was not due to peripheral vasodilatation, and this can be definitely excluded. This was based on the finding that within 3 min after antigen administration, the left ventricular end-diastolic pressure and arterial blood pressure increased, indicating pump failure. Contemporarily, electrocardiographic recordings uniformly showed signs of acute myocardial ischemia. The blood pressure started declining steadily after 4 min. Today, Dr Stephan Felix (6), the author who performed the above experiments, still believes that, in anaphylactic shock, tissue ischemia is due to disturbances of vasomotion of the coronaries (either coronary vasospasm or disturbances of the microcirculation). However, he cannot exclude fluid extravasation (personal communication, email, November 26, 2012). Other experiments (7), with isolated guinea pig hearts undergoing anaphylaxis following intra-aortic injection of antigen, have shown a prompt and prolonged decrease in coronary blood flow, an abrupt heart rate increase reaching the peak within 2 min, and a transient increase in ventricular contractile force. It has been shown also (8) that anaphylactic cardiac damage is dissociated temporarily into two sets of events: an initial primary coronary reaction caused by intracardiac release of histamine and a subsequent cardiovascular reaction secondary to systemic release of mediators. There are, currently, patients with anaphylactic cardiac shock who did not respond to intravenous fluid administration and antiallergic therapy but required coronary event treatment protocol. In a patient (9) who was stung by multiple wasps and developed type I variant of Kounis syndrome with anaphylactic shock and myocardial ischemia, treatment with 2 L of normal saline, adrenaline, hydrocortisone, and antihistamines did not have any immediate effect, and the patient recovered in a later stage with vasopressors and myocardial infarction protocol treatment. In an atopic female nurse (10) with previous atopic eczema, asthma, and allergy to milk protein, who suffered an anaphylactic reaction, hemodynamic status was unresponsive to intravenous administration of fluids such as Ringer’s acetate and antiallergic treatment with adrenaline and corticosteroids, but the patient recovered with myocardial infarction protocol treatment. It was commented that hemodynamic disturbance was most probably due to myocardial stunning leading to reduced cardiac output rather than due to fluid extravasation. In another patient with hymenoptera sting–induced anaphylactic shock (11), urgent coronary angiography revealed acute coronary thrombosis, and the patient recovered with intra-aortic balloon pump assistance and myocardial infarction treatment. Differentiating global hypoperfusion from primary tissue suppression due to mast cell mediator action on systemic arterial vasculature seems to be challenging. Combined tissue suppression from arterial involvement and peripheral vasodilatation, perhaps, occur simultaneously. Although the mechanisms of anaphylactic shock still remain to be elucidated, the above effects resemble those during endotoxin administration and postischemic hypoperfusion (3). In this aspect, the experiments of Davidson et al (1) help to understand the pathophysiology of anaphylactic shock, but further studies are needed to determine the importance of mediators of anaphylaxis in cerebral and myocardial pathobiology. Nicholas Kounis George N. Kounis George D. Soufras Andreas Mazarakis Department of Medical Sciences Patras Highest Institute of Education and Technology Patras, Grecce

Posttraumatic vasospasm and intracranial hypertension after wartime traumatic brain injury

Summary Traumatic brain injury (TBI) is associated with the severest casualties from Operation Iraqi Freedom (OIF) and Operation Enduring Freedom (OEF). From October 1, 2008 the US Army Medical Department initiated a transcranial Doppler (TCD) ultrasound service for TBI patients; included patients were retrospectively evaluated for TCD-determined incidence of posttraumatic cerebral vasospasm and intracranial hypertension after wartime TBI. Ninety patients were investigated with daily TCD studies and comprehensive TCD protocol and published diagnostic criteria for vasospasm and raised intracranial pressure (ICP) were applied. TCD signs of mild, moderate and severe vasospasms were observed in 37%, 22% and 12% of patients, respectively. TCD signs of intracranial hypertension were recorded in 62.2%, five patients (4.5%) underwent transluminal angioplasty for post-traumatic clinical vasospasm treatment and 16 (14.4%) had cranioplasty. These findings demonstrate that cerebral arterial spasm and intracranial hypertension are frequent and significant complications of combat TBI, therefore daily TCD monitoring is recommended for their recognition and subsequent management.

Accuracy of transcranial colour-coded sonography in the diagnosis of anterior cerebral artery vasospasm

Background and purposeTranscranial colour-coded sonography (TCCS) has been proven to be a method of high performance in the diagnosis of spasm of the middle cerebral artery (MCA). Relevant data concerning the anterior cerebral artery (ACA) varies amongst studies. The aim of this study was to assess the performance of TCCS in the diagnosis of spasm affecting the ACA. Material and methodsNinety-two patients (39 women and 53 men, age 51 ± 12.1 years) were examined using TCCS before cerebral angiography. Of 184 examined ACAs, only 133 arteries could be visualized due to insufficiency of the temporal acoustic window. Therefore, only 15 out of 25 arteries in which vasospasm was diagnosed with angiography (by two neuroradiologists not informed about the sonographic findings) could be included in the analysis. Receiver operating characteristic (ROC) curves were constructed for specific blood flow velocities: peak systolic (PSV), mean (M) and end-diastolic (EDV). The area under the ROC curve was used to measure the overall diagnostic performance of TCCS. ResultsThe area under the ROC curve for PSV was 0.83, which indicates good performance. The PSV threshold of 98 cm/s corresponded to maximum accuracy and was associated with 71% sensitivity vs. 88% specificity. Average systolic blood flow velocity in the vessels with vasospasm was 129 cm/s, whereas in unaffected vessels it was 76 cm/s. ConclusionsThe accuracy of TCCS in the diagnosis of ACA spasm is relatively high – the value of the area under the ROC amounts to 0.83. PSV performs best and the threshold of 98 cm/s is associated with an optimal trade-off between sensitivity and specificity.

Ruptured Aneurysm With Delayed Distal Coil Migration Requiring Surgical Treatment

A 64-year-old woman with subarachnoid hemorrhage manifesting as sudden onset of severe headache visited our hospital on post-onset day 8. Diagnostic cerebral digital subtraction angiography revealed an aneurysm located at the left internal carotid-anterior choroidal artery with diffuse cerebral arterial spasm. Coil embolization was selected because of diffuse spasm in spite of parent artery elongation at the extra-cranial portion. A small portion of the coil migrated to the parent artery, but coil embolization was successfully completed. The patient developed delayed spasm, which required arterial fasudil hydrochloride injection. After the acute phase of subarachnoid hemorrhage, the patient's symptoms disappeared. However, on day 24 after subarachnoid hemorrhage, the patient showed right hemiparesis and total aphasia, and skull radiography revealed that the migrated coil had moved into the M1 portion of the left middle cerebral artery. Craniotomy was performed to retrieve the coil and clip the aneurysm neck. However, the migrated coil could not be retrieved because of adhesion to the arterial wall. Delayed coil migration is very rare in the chronic phase.

Postpartum Cerebral Angiopathy Mimicking Hypertensive Putaminal Hematoma: A Case Report

Objective: To present an emerging clinical entity which may mimick another common entity. Methods: A 31 year-old woman complained of sudden severe headache and collapsed. She had delivered by Cesarean section one week previously. She had a normal antenatal history and did not have any evidence of hypertension. Results: Clinical examination revealed her to be in altered sensorium, GCS E2V2M5 with reduced movements on the left side. CT scan showed a large right putaminal hematoma with mass effect and midline shift. MRI also showed the hematoma but the MRV was normal. Despite antiedema measures and hyperventilation, the patient continued to deteriorate and so underwent right hemicraniectomy. MRA was done postoperatively and showed diffuse spasm of both middle cerebral arteries. A diagnosis of postpartum cerebral angiopathy was made and she was put on methylprednisolone and other antiedema measures were continued. With this she improved significantly. At one year she had residual hemiparesis but had returned to work. Four-vessel angiogram repeated 1 year later showed no arterial spasm. She later had cranioplasty to cover the defect. Conclusions: This case is presented to show that in a postpartum patient, if she presents with putaminal hematoma, postpartum angiopathy needs to be suspected and appropriate investigations and treatment, including steroids, should be given as the overall prognosis is good.

Counterpoint: Sympathetic nerve activity does not influence cerebral blood flow

It is intuitively clear that the cerebral circulation cannot take part in general cardiovascular regulation. During states of shock, where the sympathetic nervous system is activated, leading to a decrease in the perfusion of kidneys and mesenteric vascular bed, the cerebral circulation is kept

Cortical blindness—A rare complication of severe burns: A report of seven cases and review of the literature

CB is a rare complication of severe burns and, to our knowledge, there have been few reports of the condition in the English literature [2]. The principal clinical manifestation of CB is transient loss of binocular vision, with normal ocular fundi and pupillary reflexes [3,4]. Common causes of CB [3–10] include spasm of the posterior cerebral arteries, hypoventilation, hypercapnia, hypertension, hypotension, head trauma,