Evidence Of Subarachnoid Hemorrhage Research Articles

Abstract Number ‐ 68: Thrombectomy Through Persistent Trigeminal Artery In A Patient With P2 Occlusion: Case Report

Introduction Mechanical thrombectomy for distal medium vessel occlusions (DMVO) of the posterior circulation has been shown to be safe and technically feasible. Additionally, mechanical thrombectomy through a persistent trigeminal artery (PTA) for occlusions near the superior bifurcation of the basilar artery has been described before. However, the safety and efficacy of such procedures for DMVO remain unclear. We present a case of thrombectomy through a Saltzman type 1 PTA in an acute P2 occlusion. Methods A woman in her 80s with atrial fibrillation was admitted after undergoing a thrombectomy for a left M1 occlusion. Two days post‐procedure, she developed a right P2 occlusion with severe motor deficit secondary to thalamic hypoperfusion. She underwent mechanical thrombectomy through a right PTA. A balloon guide catheter (BGC) was placed in the right internal carotid artery (ICA). Initially, a 4F catheter over a 0.014 microwire was introduced but failed to navigate through the PTA. Afterward, the system was exchanged for a 5F aspiration catheter over a 0.021 microcatheter and 0.014 microwire which successfully tracked up through the PTA to the face of the clot. Aspiration alone was attempted initially, followed by the combined technique of aspiration with stent‐retriever. Results Our initial attempt to navigate the 4F catheter over the microwire through the PTA and up the basilar artery was unsuccessful as it continued to herniate into the cavernous ICA. Switching to the triaxial approach with the 5F catheter over the microsystem allowed navigation to the clot, however, aspiration alone was not sufficient to recanalize the occlusion and led to significant vasospasm which later self‐resolved. Instead, the combined technique resulted in successful thrombectomy with no untoward emboli into the right anterior circulation. The post‐procedural MRI showed multiple, scattered infarcts which were not evident on the MRI after the patient’s initial M1 thrombectomy. These infarcts involved the cerebellar and cerebral hemispheres bilaterally as well as the right thalamus. There was no evidence of subarachnoid hemorrhage on MRI. The patient continued to have significant left‐sided hemiparesis and could not be extubated, at which point the decision was made to transition to comfort measures until she passed. Conclusions Mechanical thrombectomy of a posterior circulation DMVO through a Saltzman type 1 PTA using the combined technique can be performed safely and effectively.

Abstract WP353: Assessing the Accuracy of ICD-10 Codes for Ruptured Intracranial Aneurysm Location

The adoption of ICD10 in October 2015 offers important opportunities for administrative database and EHR-based aneurysm research as it includes more than twenty distinct codes for subarachnoid hemorrhage (SAH), for the first time labeling the specific location for common sites of aneurysm rupture. Aneurysm location is a significant risk factor for rupture, but was not specified in any previous ICD classification. This has limited the value of “big-data” research for aneurysm risk modeling. Currently, it is not clear how frequently - or accurately - the codes are being used in practice. This study reviewed three years of records (10/2015-9/2018) from the UCHealth system in Colorado to assess the accuracy and utility of these codes for stroke research. Over this time, ICD10 codes for SAH (I60.x) were used a total of 5,090 times in 1,842 patients. After removing non-aneurysmal SAH (I60.8), the majority (92.7%) of the codes had no location specified (I60.7, I60.9). Of the codes with a location (I60.00-I60.6), upon review of the clinical record 9 (2.5%) did not have any evidence of subarachnoid hemorrhage, 3 (0.8%) did not have an aneurysm, and 5 (1.4%) had a pseudoaneurysm. Of the 338 verified instances of aneurysmal subarachnoid hemorrhage, 82 (24%) had multiple aneurysms and were excluded from further analysis. Within those records that had only a single aneurysm 197/256 (77%) had the location coded correctly. Of the 23% that were incorrectly coded, 1 was coded as the correct artery on the wrong side, all remaining (n=58) were the wrong artery. Although ICD10 codes offers the possibility of more advanced analysis due to the inclusion of aneurysm location, based on these data, we found that codes specifying location are frequently incorrect. Future studies are needed to validate these findings in other settings. However, researchers should be cautious about their ability to detect aneurysm location from administrative billing data using ICD10 location mapping.

Abstract WP117: Quantitative Susceptibility Mapping (QSM) and Vessel Wall Imaging (VWI) MRI Sequences in Identifying Subjects With Intracranial Aneurysms Who Have Microbleeds

Background and Purpose: Sentinel symptoms of aneurysm’s micro - hemorrhage such as sentinel headache or cranial nerve (CN) neuropathies are associated with an increased risk of subarachnoid hemorrhage (SAH). We tested a new MRI protocol that may aid the identification of microbleeds associated with sentinel symptoms in patients with negative head CTs and lumbar punctures. Methods: Twenty-eight consecutive subjects with a total of 35 aneurysms were enrolled in this pilot study between March/2018 to July/2018. All subjects presented with sentinel symptoms, no evidence of SAH on head CT or spinal puncture. The MRI protocol included: MRA with gadolinium, high-resolution MR vessel wall imaging (MRI-VWI) and MR imaging quantitative susceptibility mapping (MRI-QSM). Two blinded neuroimaging experts reviewed every image to determine evidence of vessel-wall enhancement or positive MRI-QSM signal. A third adjudicator intervened in case of disagreement. Statistical differences were determined by Student t-test, as well as Mann-Whitney U test for non-parametric variables. Results: 35 CAs (100%) were analyzed with MR-VWI, whereas only 24 CAs (77.1%) on MRI-QSM due artifact form the skull base bone ( P =0.005). Fifty percent (50%) of anterior communicating artery aneurysm were not visualized on MRI-QSM. Four subjects presented with typical sentinel headache and twenty four with some cranial neuropathy. Interobserver agreement was 100% for MRI-QSM, while 83.9% in MRI-VWI (P=0.06). Disagreements derived from the differentiation between mild and no contrast enhancement in MR-VWI. MRI-QSM had a sensitivity of 100% and a specificity of 100% in micro-hemorrhage identification. Whereas, MRI-VWI had sensitivity of 100% and specificity of 51.9%. Conclusions: MRI-QSM is a valuable tool in identifying micro-hemorrhage in patients who present with sentinel symptoms. However, its main limitation is bone artifact in aneurysms close to bone structures.

Abstract WP325: Peri-operative Neurological Complications of Valve Surgery for Infective Endocarditis Patients With Stroke

Introduction: Surgical valve repair is often delayed for infective endocarditis (IE) patients with stroke. We compared neurological outcome of early and delayed valve surgery and identified pre-surgical imaging characteristics that were associated with perioperative neurological complications. Methods: We reviewed 228 patients with acute IE diagnosed by modified Duke’s Criteria who underwent cerebral angiogram (CA) between January 2010 - December 2016 at a single center. Patients without pre-surgical CT and MRI were excluded. Date of IE diagnosis was defined as date of antibiotic initiation. Early surgery was defined as valve replacement ≤14 days from date of IE diagnosis, delayed as >14 days. Peri-operative neurological complication is any new clinical or radiologic diagnosis of ischemic or hemorrhagic stroke, and seizure. Results: 148 of 228 patients underwent valve surgery. 69 patients (46.6%) had early surgery at median 9 days after IE diagnosis, and 79 patients (53.4%) had delayed surgery at median 28 days. On pre-surgical imaging, acute to subacute ischemic stroke was seen in 81% of the early group (n=56) and 78% of the delayed group (n=62, p=0.69). However, 22.8% of patients (n=18) in the delayed group had evidence of subarachnoid hemorrhage (SAH) compared to 10.1 % of patients in the early group (n=7, p=0.04). Despite this finding, delayed group did not have higher rate of perioperative neurological complication than that of the early group (24.1% vs 13%, p=0.95). Overall, 15 surgical patients (10.1%) had perioperative neurological complications: 4 with acute ischemic stroke, 9 with ICH, 1 with both an infarct and ICH, and 3 with seizures. 33.3% of patients who had a perioperative neurological complication had evidence of SAH on pre-surgical imaging (n=6) compared to 14.6% of patients who did not have any neurological complications (n=19, p=0.012). In the group of patients with complications, SAH found prior to surgery were all cortical in the sulci, and 3 cases of SAH were associated with presence of infectious intracranial aneurysm found on pre-surgical CA. Conclusion: In IE patients with stroke, presence of sulcal SAH on pre-surgical imaging is associated with developing perioperative neurological complications irrespective of surgical timing.

Spontaneous Acute Subdural Hemorrhage with Rupture of Intracranial Aneurysm: A Series of Two Cases and Review of Literature

We present a rare series of two cases of spontaneous intracranial aneurysmal hemorrhage associated with acute subdural hematoma. One patient was having ruptured anterior communicating artery aneurysm and acute subdural hematoma with no evidence of subarachnoid hemorrhage and the other patient presented with subarachnoid hemorrhage with bleeding in subdural, intraparenchymal, and intraventricular location with rupture of posterior communicating artery aneurysm. In this report, we are describing the pathophysiology and radiological features of subdural hematoma with aneurysm bleed.

Abstract 170: Aspirin Reduces Mortality Caused by Intracranial Aneurysm Rupture in mPGES-1 Deficient Mice

Inflammation plays an important role in formation and rupture of intracranial aneurysms. Prostaglandin (PG) E2, a by-product of microsomal prostaglandin E2 synthase (mPGES)-1, is associated with inflammation and cerebrovascular dysfunction. We hypothesized that mPGES-1 deficiency protects against rupture of intracranial aneurysms. Intracranial aneurysms were induced in mPGES-1 knockout (KO) and wild-type (WT) mice with DOCA-salt hypertension and an intracranial injection of elastase. Systolic blood pressure and water intake (1% saline) was similar in WT and mPGES-1 KO mice. All WT mice survived 3 weeks after surgery and did not develop signs of subarachnoid hemorrhage (SAH). The majority of WT mice [73% (8/11)] developed aneurysmal dilatations in the cerebral arteries without evidence of SAH. In contrast, half of mPGES-1 deficient mice died or showed signs of SAH during follow-up (P<0.05). Postmortem analysis showed SAH in 56% (9/16) of mPGES-1 deficient mice. Unruptured aneurysms with no evidence of SAH were found in 25% (4/16) of mPGES-1 deficient mice. Subcutaneous infusion of PGE2 (1 mg/kg/d) to mPGES-1 KO mice did not appear to attenuate mortality or intracranial aneurysm rupture (p>0.05). Another group of mPGES-1 KO mice were treated with aspirin (6 mg/kg/d) or vehicle (water) by gavage since day 2 after surgery. Mortality caused by symptomatic aneurysm rupture was significantly reduced in aspirin (25% (3/12) vs vehicle (58% (7/12)) treated mPGES-1 KO mice (P<0.05). In conclusion, we found that genetic deficiency of mPGES-1 is associated with increased aneurysm rupture (p<0.01) and mortality (p<0.05) in a mouse model of intracranial aneurysms. Aspirin treatment significantly reduced mortality in mPGES-1 KO mice (P<0.05). Therefore, mPGES-1 and aspirin appear to play a protective role against rupture of intracranial aneurysms in mice.

Critical role of TNF-α in cerebral aneurysm formation and progression to rupture.

BackgroundAlterations in TNF-α expression have been associated with cerebral aneurysms, but a direct role in formation, progression, and rupture has not been established.MethodsCerebral aneurysms were induced through hypertension and a single stereotactic injection of elastase into the basal cistern in mice. To test the role of TNF-α in aneurysm formation, aneurysms were induced in TNF-α knockout mice and mice pretreated with the synthesized TNF-α inhibitor 3,6′dithiothalidomide (DTH). To assess the role of TNF-α in aneurysm progression and rupture, DTH was started 6 days after aneurysm induction. TNF-α expression was assessed through real-time PCR and immunofluorescence staining.ResultsTNF-α knockout mice and those pre-treated with DTH had significantly decreased incidence of aneurysm formation and rupture as compared to sham mice. As compared with sham mice, TNF-α protein and mRNA expression was not significantly different in TNF-α knockout mice or those pre-treated with DTH, but was elevated in unruptured and furthermore in ruptured aneurysms. Subarachnoid hemorrhage (SAH) occurred between 7 and 21 days following aneurysm induction. To ensure aneurysm formation preceded rupture, additional mice underwent induction and sacrifice after 7 days. Seventy-five percent had aneurysm formation without evidence of SAH. Initiation of DTH treatment 6 days after aneurysm induction did not alter the incidence of aneurysm formation, but resulted in aneurysmal stabilization and a significant decrease in rupture.ConclusionsThese data suggest a critical role of TNF-α in the formation and rupture of aneurysms in a model of cerebral aneurysm formation. Inhibitors of TNF-α could be beneficial in preventing aneurysmal progression and rupture.

MPGES‐1 deficiency increases mortality and aneurysm rupture in a mouse model of intracranial aneurysms

Studies in humans and mice suggest that inflammation plays an important role in formation and rupture of intracranial aneurysms. Prostaglandin (Pg) E2, a byproduct of microsomal prostaglandin E2 synthase (mPGES)‐1, is associated with inflammation and cerebrovascular dysfunction. We hypothesized that mPGES‐1 deficiency protects against rupture of intracranial aneurysms. Intracranial aneurysms were induced in mPGES‐1 KO and WT mice with DOCA‐salt hypertension and an intracranial injection of elastase. Systolic blood pressure and water intake (1% saline) was similar in WT and mPGES‐1 KO mice. Body weight did not change in any group during the experiment. All WT mice survived 3 weeks after the surgery and did not develop signs of subarachnoid hemorrhage (SAH). 73% (8/11)of WT mice developed aneurysmal dilatations in the cerebral arteries without evidence of SAH. In contrast, half of mPGES‐1 deficient mice died or showed signs of SAH during follow‐up. Postmortem analysis showed SAH in 56% (9/16)of mPGES‐1 deficient mice. Unruptured aneurysms with no evidence of SAH were found in 25% (4/16)of mPGES‐1 deficient mice. In conclusion, we found that genetic deficiency of mPGES‐1 is associated with increased aneurysm rupture (p<0.01)and mortality (p<0.05) in a mouse model of intracranial aneurysms. mPGES‐1 appears to play a protective role against rupture of intracranial aneurysms in mice.

Resection of an anterior spinal cord AVM through a far-lateral approach.

A small arteriovenous malformation near the craniocervical junction with contributions from the anterior spinal artery was discovered in a young developmentally-delayed woman after she presented with altered mental status and evidence of subarachnoid hemorrhage. The malformation could not be completely treated with endovascular therapy, so it was resected through a far-lateral approach. This stereoscopic video demonstrates how to gain the exposure needed to address a lesion in this area. The video can be found here: http://youtu.be/ByjPGm_eXLc .

Endovascular Treatment of Acute Intracerebral Artery Occlusions with the Solitaire Stent: Single-Centre Experience with 108 Recanalization Procedures

Background and Purpose: Stent retrievers are currently displacing ‘classical’ thrombectomy devices for recanalization in acute ischaemic stroke. The aim of our study was to show the procedural efficacy and safety of the Solitaire stent retriever as part of our multimodality endovascular approach in the treatment of ischaemic stroke. Methods: Between March 2008 and December 2009, 104 patients [53 females (51%), 51 males (49%), mean age 67.3 years (range 31–96)] with 108 territorial occlusions were treated with the Solitaire stent alone or in conjunction with other endovascular stroke devices. All patients were referred to our service after clinical evaluation by a team of stroke neurologists as part of our standard treatment algorithm with 0.9 mg/kg i.v. recombinant tissue-type plasminogen activator and endovascular continuation of treatment in CT angiography-proven main branch occlusion. The time of angiography was defined as the moment of groin puncture. Final reperfusion success was rated according to the Thrombolysis in Cerebral Infarction (TICI) scale; the first persistent Thrombolysis in Myocardial Infarction (TIMI) 2/3 reperfusion was used for time-to-reperfusion measures. Results: Fifty-eight patients were treated in conjunction with intravenous lysis, 32/104 received intra-arterial lytics. Twenty-five territories were treated with the Solitaire alone; the remaining 83 were treated with a combination of mechanical thrombectomy devices or aspiration thrombectomy followed by or in conjunction with the Solitaire. The most frequent combination was a proximal aspiration/distal access catheter and Solitaire (62/108). In 15/108 procedures, temporary stenting without thrombectomy was performed. Eighty-three successful thrombectomy attempts were performed in the remaining 93 territories. The mean number of Solitaire passes was 2.46 (median 2, max. 12). The mean time from onset to reperfusion was 265 min (range 56–1,031), median 230 min; the mean angio-to-reperfusion time was 47 min (5–186), median 38.5 min. A subanalysis showed a significant reduction of the angio-to-reperfusion time when the Solitaire was used (48.7 vs. 68 min). The rate of final TICI 2b/3 reperfusion was 79% for the anterior and 77.9% for the posterior circulation (TIMI 2/3 for both: 92.5%). During or after the first deployment of the Solitaire, 72.8% showed TIMI 2/3 reperfusion. The mean National Institute of Health Stroke Scale score on admission was 15.3 and decreased by 7.8 points at clinical discharge. The overall mortality at discharge was 16% in the anterior and 47.8% in the posterior circulation group. There were 2 cases of periprocedural intracranial haemorrhage, unrelated to the Solitaire, 6 patients had evidence of subarachnoid haemorrhage, 2 potentially related to the Solitaire deployment. In 4/108 territories, thrombus migration to previously unaffected territories was noted. Vasospasm was seen in 13% of the target vessels. One device was inadvertently detached during retrieval. All these complications had no clinical consequence. Conclusions: Our single-centre experience proves the technical feasibility and safety of the Solitaire for the treatment of acute intracranial vessel occlusion and approves previous reports with smaller patient numbers. Further multicentre studies with a randomized and prospective design will be necessary to verify the results.

A Reminder for a Very Rare Entity: Massive Tongue Swelling after Posterior Fossa Surgery

The purpose of this study is to report a case of presumably neurogenic macroglossia that occurred after surgical trapping of a vertebral artery (VA)-posteroinferior cerebellar artery aneurysm, and to analyze its potential pathogenesis. A 53-year-old woman who suffered from headaches and intermittent loss of consciousness but without evidence of subarachnoid hemorrhage was admitted. Magnetic resonance imaging and angiography showed an irregular aneurysm in the fourth segment of a left dominant VA. Surgical treatment was indicated after discussion with the neuroradiology team. During surgery, in the prone position the aneurysm ruptured. The patient became hemodynamically instable. On the first postoperative day, macroglossia appeared and remained for 3 weeks until spontaneous regression. Macroglossia is a rare complication following neurosurgical procedures with very few cases reported so far. It has been attributed to the sitting position and venous flow congestion. We illustrate a case of macroglossia, which occurred following surgery in the prone position. Its etiology remains speculative, but a neurogenic explanation seems most plausible.

Rapid resolution of acute subdural hematoma: A case report and review of literature

Acute traumatic subdural hematoma is a common condition. Cases of rapid resolution of acute subdural hematoma have seldom been reported in the literature. We are reporting one such case of 53 year-old-male admitted after road traffic accident. Patient became unconscious immediately after the accident. Computed Tomography (CT) done after one hour of accident showed an acute hyperdense subdural hematoma with low density area between skull and hematoma and subarachnoid hemorrhage (SAH). He improved quite rapidly during transportation and became conscious at the time of admission in our hospital. Repeat CT scan done after 7 hours showed marked resolution of hematoma but there was evidence of subarachnoid hemorrhage (SAH). Another CT scan done after 72 hours of injury showed complete resolution of hematoma with evidence of SAH. Possible mechanism of spontaneous resolution of the hematoma in our case was dilution and washing-out of hematoma by the cerebrospinal fluid due to an arachnoid tear. Clinician should suspect possibility of resolving hematoma if CT scan shows presence of SAH and hypodensity between hematoma and skull. Such patients who do not deteriorate while awaiting surgery because of delay due to any reason should get a repeat CT scan before planning any surgical intervention.

Ruptured Internal Carotid Artery Bifurcation Aneurysm Presenting With Only Intracerebral Hemorrhage Without Subarachnoid Hemorrhage -Case Report-

A 55-year-old man presented with intracerebral hemorrhage (ICH) without subarachnoid hemorrhage (SAH) manifesting as acute onset of consciousness disturbance and right hemiparesis. Computed tomography showed ICH mainly localized in the left putamen, but no evidence of SAH. Magnetic resonance angiography demonstrated a cerebral aneurysm originating from the bifurcation of the left internal carotid artery, which was considered to be responsible for the ICH. The patient underwent emergent intravascular surgery for coil embolization of the aneurysm, and his neurological symptoms gradually recovered with rehabilitation after surgery. Although ICH without SAH is a rare presentation of cerebral aneurysm, ruptured cerebral aneurysm should be considered as a potential cause of ICH. The localization and extent of ICH may be suggestive of latent cerebral aneurysm in such cases.

A High CSF Signal on FLAIR: It is Not Always Blood

We describe a patient with progressive neurologic deficit due to middle cerebral branch occlusion. Temporary partial balloon occlusion of the abdominal aorta led to an increased signal in the subarachnoid space on fluid-attenuated inversion recovery images with no evidence of subarachnoid hemorrhage. After spontaneous recanalization, the increased signal of the subarachnoid space returned to normal. We assume that signal changes in the subarachnoid space were due to a temporary increase in blood volume in the superficial brain vessels.

Cerebral venous sinus thrombosis as a rare cause of thunderclap headache and nonaneurysmal subarachnoid haemorrhage

Sirs: In a clinical setting, isolated thunderclap headache is commonly assumed to be benign in origin once subarachnoid haemorrhage (SAH) has been excluded [1]. However, cerebral venous sinus thrombosis (CVST) is an infrequent, alternative cause of sudden-onset headache and is not conclusively excluded by normal conventional CT and LP. CVST is also a recognised rare cause of SAH. Here, we report a case of CVST presenting with thunderclap headache and complicated by delayed SAH. A previously well 53-year-old woman presented with spontaneous, sudden-onset occipital headache as her sole symptom. Neurological examination including fundoscopy was normal, with no evidence of meningism. Acute head CT and subsequent LP performed 16 hours after onset were unremarkable (opening pressure 19 cm, CSF acellular with no bilirubin detectable on spectrophotometry). The headache resolved completely within 24 hours and the patient was discharged with a diagnosis of primary thunderclap headache. The following day, she represented with sudden-onset headache at rest accompanied by mild neck stiffness. Her symptoms resolved before a further suddenonset headache occurred two days later. Examination remained normal throughout. Repeat, unenhanced head CT demonstrated a small, high left frontal SAH along the cranial convexity without involvement of the basal cisterns (Fig. 1a). CT angiography detected no arterial aneurysm, but its venous phase showed changes suggestive of superior sagittal sinus thrombosis, which was confirmed on MR venography (Fig. 1b). Screening for secondary causes of thrombosis was negative. She was initially treated with intravenous unfractionated heparin to allow rapid reversal in case of rebleeding, before being warfarinised under cover from low molecular weight heparin. She remained well at follow-up six months later. Repeat MR angiography showed resolution of the superior sagittal sinus thrombosis, with no other vascular or brain parenchymal abnormalities. Thunderclap headache is an unusual presentation of CVST, perhaps seen in fewer than 20 % of cases [2]. Rarely, there may be no concomitant findings to suggest the presence of a CVST, such as focal neurological signs, seizures or features of raised intracranial pressure. Most patients with CVST have a raised opening pressure and abnormal CSF constituents, but absence of these features does not conclusively rule out the diagnosis. In a previous series of 38 cases, nine patients had both opening pressure and CSF constituents measured, and in one of them all parameters were normal [3]. SAH is a very rare complication of cerebral venous thrombosis, with only 30 cases reported to date. It has been suggested that venous intraparenchymal haemorrhages may rupture into the subarachnoid space, thus causing sudden-onset headache in CVST [2, 4]. However, we hypothesise that our patient’s first headache was caused by the CVST, as there was no evidence of SAH on initial brain CT and bilirubin was not detectable in the CSF. The second or third episode of headache may have been caused by SAH. LETTER TO THE EDITORS

Severe brainstem compression by an unruptured giant vertebral aneurysm – An autopsy case

We describe an autopsy case of sudden unexpected death due to severe brainstem compression by an unruptured giant vertebral aneurysm. A 71-year-old male was found dead in his bedroom. The forensic autopsy revealed no severe trauma leading to his death. On internal examination, a giant intracranial aneurysm (3.4 × 2.6 × 2.7 cm) was observed on the trunk of the right vertebral artery. The aneurysm compressed the right side of the lower one-third of the pons and adjacent medulla oblongata. On sectioning, almost all of the aneurysm lumen was filled with a firm, clearly laminated organized thrombus. There was no evidence of subarachnoid hemorrhage. Histopathological analyses revealed congestion and hypoxic tissue changes in all organs examined. In microscopic sections of the giant vertebral aneurysm, thick fibrotic walls, intimal hyperplasia and organized thrombi in the lumen were found. Lots of intrathrombotic clefts with fresh erythrocytes were also observed. Moreover, Elastica van Gieson staining revealed fragmentation and disruption of the intimal elastic lamina in the aneurysmal wall. Collectively, we considered that some triggers in his daily life, including head rotation, might have caused the rapid onset of respiratory disturbance due to severe brainstem compression by a giant vertebral aneurysm.

Diffuse cerebral oedema mimicking subarachnoid haemorrhage on computed tomography

A 62-year-old man with a history of petrol consumption was admitted to the accident and emergency department of an adjacent district general hospital by paramedics. He complained of headache and difficulty in breathing. On admission his Glasgow Coma Scale was 10/15 which rapidly deteriorated to 4/15. An unenhanced computed tomography (CT) scan was performed immediately which showed obliteration of basal cisterns consistent with brainstem oedema. He was mechanically ventilated with inotropic support and then transferred to the intensive care unit of the authors' institution. Relevant past history included alcohol abuse, manic depressive psychosis and carbamazepine overdose. Following transfer, sedation was withdrawn and the patient reassessed. He had fixed dilated pupils, no respiratory effort, absent gag reflex and response to pain. He was also hypernatraemic with a serum sodium level of 170 mmol/litre (normal range 133–144 mmol/litre). Toxicology for paracetamol and salicylates was negative. A repeat unenhanced CT scan was performed at this stage. This showed high attenuation in the tentorium (Figure 1a), basal cisterns (Figures 1b and c) and in the sylvian fissures (Figure 1d). There was no history of injection of intravascular or intrathecal iodinated contrast media. This was initially interpreted as subarachnoid haemorrhage. On subsequent review, the diagnosis was changed to diffuse cerebral oedema. In view of a failing brainstem and after discussion with the patient's family, treatment was withdrawn. A post mortem examination performed by the coroner showed no evidence of subarachnoid haemorrhage.

Warning Headache of Subarachnoid Hemorrhage and Infarction due to Vertebrobasilar Artery Dissection

The authors describe the clinical features of headache in patients with vertebrobasilar artery dissection (VBAD) and emphasize the importance of recognition of warning headaches preceding subarachnoid hemorrhage. Headache in VBAD is already recognized, but the natural history and clinical features of the warning headache have not been well elucidated. The clinical features of 30 patients with VBAD were analyzed retrospectively. Of the 30 VBAD patients, 16 presented with subarachnoid hemorrhage and 14 with ischemia. Headache (without any other symptoms or signs) was detected in 70% of patients with subarachnoid hemorrhage and 50% of patients with infarction. The headache started acutely, was localized to the occiput or nape of the neck, was sharp and severe in intensity, and was different from any previously experienced headaches. The interval from onset of headache to diagnosis of subarachnoid hemorrhage or infarction was 1 to 10 days. Three patients had sudden severe warning headaches without any evidence of subarachnoid hemorrhage at initial presentation and deteriorated within 24 hours due to subarachnoid hemorrhage, demonstrated later on computed tomography. Angiographic findings of patients with warning headaches were nonspecific compared with those of patients without headache. The present study confirms a high frequency of headache in patients with VBAD. Sudden severe occipital and nuchal pain, even without subarachnoid hemorrhage or any neurologic deficit, should be considered as a warning sign of subarachnoid hemorrhage. Computed tomography, magnetic resonance imaging, and magnetic resonance angiography should be performed urgently for screening of patients with a warning headache to prevent resultant life-threatening major vascular events.

Occlusion of the posterior communicating artery mimicking cerebral aneurysm: Case report

We report a rare case of posterior communicating artery occlusion mimicking a cerebral aneurysm. A 62-year-old man was admitted to Towakai Hospital with sudden onset of left motor weakness. He had developed thunderclap headache five days before. Computed tomographic scan and lumbar tap were negative for subarachnoid hemorrhage (SAH). Digital subtraction angiography and three-dimensional computed angiography showed aneurysmal protrusion at the junction of the right internal carotid (IC) artery and posterior communicating artery (PcomA). Because minor bleeding from IC-PcomA junction aneurysm was strongly suspected, a pterional craniotomy was performed. At surgery, there was no evidence of SAH but the PcomA was occluded at the peripheral portion. Several perforators arose from the proximal portion of the PcomA. An aneurysmal protrusion especially without a prominent PcomA does not always indicate an IC-PcomA aneurysm. In diagnosing protruding vascular lesions at the bifurcation between the IC-PcomA, not only infundibular dilatation but also occlusion of the PcomA should be considered if the PcomA is not visualized.

Sonographically detected subarachnoid hemorrhage: an independent predictor of neonatal posthemorrhagic hydrocephalus?

Blood from an intraventricular hemorrhage (IVH) can collect in the basilar cisterns and cause ventriculomegaly and eventual need for ventriculoperitoneal (VP) shunt. We looked for sonographic evidence of subarachnoid hemorrhage (SAH) in three basal cisterns and in the Sylvian fissure of 82 infants with IVH, 30 of whom had ventriculomegaly. We found that ultrasonographically diagnosed SAH and measurement of ventricular blood volume predict ventriculomegaly and need for VP shunt.