Ruptured Proximal Lenticulostriate artery Fusiform Aneurysm Presenting with Subarachnoid Hemorrhage: Case Report

Neurosurgery ◽  
2007 ◽  
Vol 60 (5) ◽  
pp. E949-E949 ◽  
Author(s):  
Christopher S. Eddleman ◽  
Daniel Surdell ◽  
Glen Pollock ◽  
H. Hunt Batjer ◽  
Bernard R. Bendok
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Basal Ganglia ◽  
Sudden Onset ◽  
Neurological Deficits ◽  
Fusiform Aneurysm ◽  
Cerebral Angiogram ◽  
Computed Tomographic ◽  
Superior Surface ◽  
Lenticulostriate Artery ◽  
Safe Approach

Abstract OBJECTIVE Lenticulostriate artery aneurysms are rare. When present, distal locations in and around the basal ganglia are more common and often present with intraparenchymal hemorrhage when ruptured. We present a very rare case of a ruptured proximal lenticulostriate fusiform aneurysm presenting with subarachnoid hemorrhage. CLINICAL PRESENTATION We report the case of a 31-year-old healthy man who presented after the sudden onset of headache, nausea, and lethargy without neurological deficits. Cranial computed tomographic scanning demonstrated diffuse subarachnoid hemorrhage, and a cranial computed tomographic angiogram demonstrated a vascular irregularity on the superior surface of the left distal M1 trunk of the middle cerebral artery. A cerebral angiogram demonstrated a left proximal lenticulostriate fusiform aneurysm without evidence of moyamoya-like vessels or vasculitis. No other pathology or infectious etiology was noted. INTERVENTION Endovascular therapy was deemed unsafe, and microsurgical exploration and intervention was the more favorable and safe approach. A standard left pterional craniotomy was performed and the afferent lenticulostriate vessel into the fusiform aneurysm was visualized. Temporary clips were applied to the proximal and distal M1 trunk and miniclips were applied across the afferent portion and fundus of the aneurysm, thus sacrificing the parent lenticulostriate artery. A postoperative computed tomographic scan demonstrated an area of hypodensity in the left basal ganglia. The patient's postoperative right facial and upper extremity weakness improved to normal several days after aneurysmal clipping. CONCLUSION This is the first report of a ruptured proximal lenticulostriate artery fusiform aneurysm, which presented as subarachnoid hemorrhage in a healthy patient without an underlying vascular disease.

Primary Treatment of a Blister-like Aneurysm with an Encircling Clip Graft: Technical Case Report

2006 ◽  
Vol 59 (suppl_1) ◽  
pp. ONS-E168-ONS-E168 ◽  
Author(s):  
Raymond F. Sekula ◽  
David B. Cohen ◽  
Matthew R. Quigley ◽  
Peter J. Jannetta
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Carotid Artery ◽  
Internal Carotid Artery ◽  
Current Practice ◽  
Internal Carotid ◽  
Primary Treatment ◽  
Sudden Onset ◽  
Cerebral Angiogram ◽  
Computed Tomographic

Abstract OBJECTIVE: Blister-like aneurysms at nonbranching sites in the supraclinoid portion of the internal carotid artery are a rare but important cause of subarachnoid hemorrhage. We report a case of subarachnoid hemorrhage caused by a ruptured blister-type aneurysm, review the pertinent literature, and hope to remind readers of the wisdom of the use of an encircling clip as the primary treatment of these challenging lesions. CLINICAL PRESENTATION: A 41-year-old woman presented with sudden onset of headache. An admission computed tomographic (CT) scan revealed thick and diffuse subarachnoid hemorrhage involving primarily the carotid cistern and the proximal left sylvian fissure. A cerebral angiogram was initially interpreted as absent for aneurysm, but a follow-up angiogram performed 1 week later confirmed an enlarging aneurysm. INTERVENTION: A craniotomy with placement of an encircling clip graft around a blister-like aneurysm was performed. CONCLUSION: Although Sundt advocated the encircling clip graft for the blister-type aneurysm almost 40 years ago, use of an encircling clip graft in the treatment of blister-like aneurysms of the supraclinoid portion of the internal carotid artery seems to be reserved as a secondary or “rescue” measure in current practice. Neurosurgeons must familiarize themselves with this distinct entity (the blister-type aneurysm), recognize the possible risks associated with parallel clipping, and consider the use of an encircling clip graft as the primary treatment.

PERIMESENCEPHALIC NONANEURYSMAL SUBARACHNOID HEMORRHAGE CAUSED BY JUGULAR VENOUS OCCLUSION

Neurosurgery ◽  
2008 ◽  
Vol 63 (6) ◽  
pp. E1202-E1203 ◽  
Author(s):  
Meharpal S. Sangra ◽  
Evelyn Teasdale ◽  
Mohammed A. Siddiqui ◽  
Kenneth W. Lindsay
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Ct Angiography ◽  
Venous Occlusion ◽  
Sudden Onset ◽  
Jugular Veins ◽  
Cerebral Angiogram ◽  
Computed Tomographic ◽  
The Right ◽  
Nonaneurysmal Subarachnoid Hemorrhage

Abstract OBJECTIVE The cause of perimesencephalic nonaneurysmal subarachnoid hemorrhage remains unknown. We describe a patient in whom jugular venous occlusion preceded the occurrence of perimesencephalic nonaneurysmal subarachnoid hemorrhage. This finding supports the theory that the source of the hemorrhage is venous in origin. CLINICAL PRESENTATION A 25-year-old man presented with sudden onset of headache after his head was held in a headlock during a playful fight 48 hours before the ictus. His computed tomographic (CT) scan on admission demonstrated a perimesencephalic pattern of subarachnoid hemorrhage. CT angiography excluded the presence of an underlying aneurysm or vascular malformation but showed bilateral jugular venous obstruction with hematoma surrounding the right internal jugular vein. Magnetic resonance imaging and a 4-vessel cerebral angiogram confirmed the CT angiographic findings. INTERVENTION The patient was observed as an inpatient and had no complication of his hemorrhage. Follow-up at 5 months with CT angiography showed resolution of his neck hematoma and reopening of his internal jugular veins. CONCLUSION The presence of acute jugular venous occlusion as a cause of perimesencephalic nonaneurysmal subarachnoid hemorrhage supports a venous origin of hemorrhage.

scholarly journals Fusiform Lenticulostriate Artery Aneurysm with Subarachnoid Hemorrhage: The Role for Superselective Angiography in Treatment Planning

2010 ◽  
Vol 16 (3) ◽  
pp. 259-263 ◽  
Author(s):  
P.S. Kochar ◽  
W.F. Morrish ◽  
M.E. Hudon ◽  
J.H. Wong ◽  
M. Goyal
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Treatment Planning ◽  
Artery Aneurysm ◽  
Cerebral Angiogram ◽  
Perforating Artery ◽  
Ct Angiogram ◽  
Superselective Angiography ◽  
Lenticulostriate Artery ◽  
The Right ◽  
Exact Origin

Aneurysms of the lenticulostriatal perforating arteries are rare and either involve the middle cerebral artery-perforator junction or are located distally in basal ganglia. We describe a rare ruptured fusiform lenticulostriatal perforating artery aneurysm arising from a proximal M2 MCA branch, discerned on superselective microcatheter angiography, presenting solely with subarachnoid hemorrhage (SAH). A 50-year-old previously healthy man presented with diffuse SAH and negative CT angiogram. Cerebral angiogram demonstrated a 2 mm fusiform aneurysm presumably arising from the right lateral lenticulostriate perforator but the exact origin of the perforator was unclear. Superselective angiography was required to precisely delineate the aneurysm and its vessel of origin and directly influenced treatment planning (surgical trapping). Superselective microcatheter angiography provides both an option for endovascular therapy as well as more accurate delineation for surgical planning for these rare aneurysms.

scholarly journals Mechanical Thrombectomy of Primary Distal Anterior Cerebral Artery Occlusion: A Case Report

2019 ◽  
Vol 11 (3) ◽  
pp. 265-270 ◽  
Author(s):  
Hironori Haruyama ◽  
Junji Uno ◽  
Kenta Takahara ◽  
Yosuke Kawano ◽  
Naoki Maehara ◽  
...  
Keyword(s):  
Case Report ◽  
Cerebral Artery ◽  
Mechanical Thrombectomy ◽  
Anterior Cerebral Artery ◽  
Rare Condition ◽  
Computed Tomographic Angiography ◽  
Artery Occlusion ◽  
Sudden Onset ◽  
Neurological Deficits ◽  
Computed Tomographic

Objective: Primary anterior cerebral artery (ACA) occlusion is a rare condition and sometimes leads to significant neurological deficits. We herein report on the efficacy of mechanical thrombectomy (MT) in treating the distal ACA occlusion in a clinical setting. Case Presentation: A 76-year-old woman presented with a sudden onset of right hemiparesis. Computed tomographic angiography and perfusion imaging and subsequent analysis with RAPID software revealed acute left ACA occlusion with salvageable penumbra. The patient obtained a score of 11 on the National Institutes of Health Stroke Scale. MT was performed for occlusion of the left ACA (A4), and successful reperfusion (Thrombolysis in Cerebral Infarction score of 3) was achieved on the first attempt using a stent retriever. The patient’s recovery progressed well, and she was discharged 13 days after admission with a modified Rankin Scale score of 1. Conclusion: This case report demonstrates the clinical efficacy, safety, and favorable clinical outcome of treating a primary distal ACA occlusion with MT.

Coating the Wall of an Injured Intracranial Carotid Artery During Tumor Removal With N-Butyl-2-Cyanoacrylate: Technical Case Report

2006 ◽  
Vol 59 (suppl_4) ◽  
pp. ONS-E484-ONS-E485
Author(s):  
Flavio Requejo ◽  
Martin Schumacher ◽  
Vera van Velthoven
Keyword(s):  
Magnetic Resonance ◽  
Carotid Artery ◽  
Residual Tumor ◽  
Artery Occlusion ◽  
Neurological Deficits ◽  
Severe Bleeding ◽  
Cerebral Angiogram ◽  
Computed Tomographic ◽  
Balloon Test Occlusion ◽  
The Right

Abstract OBJECTIVE: Carotid artery injury close to the clinoid process is difficult to repair, and is even more so when the vessel is firmly attached to a calcified tumor. We treated a patient with an intraoperative carotid lesion by coating the vessel wall with N-butyl-2-cyanoacrylate (NBCA). CLINICAL PRESENTATION: A 7-year-old boy was referred to our clinic with a 3-month history of somnolence, apathy, and headache. Neurological examination revealed bitemporal hemianopsia. The cranial magnetic resonance imaging and computed tomographic scans showed a sellar and suprasellar calcified mass with heterogeneous contrast enhancement, a cyst component in the upper part of the tumor displaced upward and back from the mesen-cephalic and diencephalic structures. INTERVENTION: The patient underwent a pterional craniotomy. Using a microsurgical technique, the suprasellar part of the craniopharyngioma was removed. In an attempt to dissect the calcified mass from the carotid artery on the right side, the vessel was unintentionally injured, followed by severe bleeding. Temporary occlusion and suturing of the vessel was impossible because of the overlying hard mass. To avoid a permanent occlusion, we decided to coat the injured artery wall with 100% NBCA. For this, 0.5 ml of NBCA was distributed on the surface of the injured segment and surrounding subarach-noid space by injection through a needle. An excellent hemostasis could be obtained immediately after coating. The patient woke up with no new neurological deficits. A digital cerebral angiogram obtained a few days after the procedure did not show vasospasm, stenosis, or pseudoaneurysm in the supraclinoidal segment of the carotid artery. A magnetic resonance angiogram obtained 3 years later showed a normal shape of the internal carotid artery and a stable residual tumor without inflammatory signs. The child is now attending school and is under hormonal therapy. CONCLUSION: For hemostatic purposes, the technique of coating an injured arterial wall with NBCA may be useful in cases in which a microsuture is impossible and a permanent artery occlusion is unwanted because of a risk of an ischemic stroke. It could serve as a transitory measure until a microsurgical bypass or the balloon test occlusion tolerance allow the trapping of the affected artery.

Brainstem Infarction after Delayed Thrombosis of a Stented Vertebral Artery Fusiform Aneurysm: Case Report

Neurosurgery ◽  
2002 ◽  
Vol 51 (5) ◽  
pp. 1280-1285 ◽  
Author(s):  
Elad I. Levy ◽  
Alan S. Boulos ◽  
Bernard R. Bendok ◽  
Stanley H. Kim ◽  
Adnan I. Qureshi ◽  
...  
Keyword(s):  
Vertebral Artery ◽  
Stent Placement ◽  
Sudden Onset ◽  
Left Vertebral Artery ◽  
Fusiform Aneurysm ◽  
Parent Vessel ◽  
Brainstem Infarction ◽  
Computed Tomographic ◽  
Cerebellar Artery ◽  
Intracranial Circulation

Abstract OBJECTIVE AND IMPORTANCE Recent technological advances have provided clinicians with stents that can be navigated throughout the tortuous proximal vessels of the posterior intracranial circulation. There have been few reports of fusiform and wide-necked aneurysms treated with stents. Of the known risks involved in stent placement in the intracranial circulation, delayed stent thrombosis has not been well described. CLINICAL PRESENTATION A 34-year-old man who experienced the sudden onset of a severe headache with increasing lethargy was found on computed tomographic imaging to have a subarachnoid hemorrhage. Angiography revealed a left vertebral artery fusiform aneurysm that incorporated the posteroinferior cerebellar artery origin. INTERVENTION A low-porosity Magic Wallstent (Boston Scientific, Natick, MA) was placed in the left vertebral artery across the aneurysm and the origin of the posteroinferior cerebellar artery. Angiography performed 9 days later revealed significant reduction in filling of the aneurysm. The patient returned 3 months after stent placement with severe neurological deterioration from a brainstem infarction caused by complete thrombotic occlusion of the left vertebral artery at the stented segment of the vessel. CONCLUSION Stenting of fusiform aneurysms has provided an alternative to surgical clipping or parent vessel reconstruction. With the increasing frequency of intracranial stent placement for various cerebrovascular disease entities, we must become aware of potential complications associated with these procedures. Such awareness may influence decision-making processes regarding treatment and follow-up care.

Intravascular Graft Stent Treatment of a Ruptured Fusiform Dissecting Aneurysm of the Intracranial Vertebral Artery: Technical Case Report

Neurosurgery ◽  
2002 ◽  
Vol 50 (1) ◽  
pp. 213-217 ◽  
Author(s):  
Juan Carlos Chiaradio ◽  
Luis Guzman ◽  
Lucio Padilla ◽  
Maria Paula Chiaradio
Keyword(s):  
Vertebral Artery ◽  
Dissecting Aneurysm ◽  
Neurological Deficits ◽  
Endovascular Procedure ◽  
Upper Cervical Spine ◽  
Difficult Case ◽  
Fusiform Aneurysm ◽  
Prepontine Cistern ◽  
Computed Tomographic ◽  
Arterial Lumen

ABSTRACT OBJECTIVE AND IMPORTANCE An innovative stenting technique to treat a difficult case of a fusiform aneurysm of the intracranial vertebral artery (VA), with restoration of the vessel lumen, is described. CLINICAL PRESENTATION A 58-year-old patient experienced sudden pain in the upper cervical spine, followed by a severe headache. He underwent computed tomographic evaluation, which demonstrated subarachnoid hemorrhage in the prepontine cistern. A fusiform aneurysm of the distal right VA and critical stenosis of the left VA were detected in digital subtraction angiograms. The patient experienced a new subarachnoid hemorrhaging episode, and urgent endovascular treatment was planned. INTERVENTION The patient underwent angioplastic and stenting procedures in the left VA, with good results. Forty-eight hours later, an endovascular procedure was performed to treat the right VA aneurysm. We decided to use a graft stent (Jostent graft stent; Jomed, Conroe, TX) instead of a balloon to preserve the arterial lumen. The complete procedure was well tolerated by the patient, and he was discharged, without symptoms, 48 hours later. CONCLUSION The patient was discharged, without neurological deficits, 48 hours after completion of the endovascular procedure, with clopidogrel (75 mg/d) and aspirin (325 mg/d) therapy. This treatment was discontinued after 4 weeks. According to our search of the medical literature, this is the first clinical case in which an intracranial fusiform aneurysm was permanently sealed with a graft stent.

scholarly journals Traumatic subarachnoid hemorrhage, basal ganglia hematoma and ischemic stroke caused by a torn lenticulostriate artery

2011 ◽  
Vol 154 (1) ◽  
pp. 59-62 ◽  
Author(s):  
Christian Fung ◽  
Werner J. Z’Graggen ◽  
Jürgen Beck ◽  
Jan Gralla ◽  
Stephan M. Jakob ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Subarachnoid Hemorrhage ◽  
Basal Ganglia ◽  
Traumatic Subarachnoid Hemorrhage ◽  
Lenticulostriate Artery

Determination of Irreversible Ischemia by Xenon-Enhanced Computed Tomographic Monitoring of Cerebral Blood Flow in Patients with Symptomatic Vasospasm

Neurosurgery ◽  
1989 ◽  
Vol 24 (3) ◽  
pp. 368-372 ◽  
Author(s):  
Howard Yonas ◽  
Laligam Sekhar ◽  
David W. Johnson ◽  
David Gur
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Neurological Deficits ◽  
Noninvasive Technique ◽  
Computed Tomographic ◽  
Symptomatic Vasospasm ◽  
Cortical Regions ◽  
Enhanced Computed Tomography

Abstract In patients with subarachnoid hemorrhage, delayed neurological deficits, often followed by infarction, are believed to result from ischemia caused by vasospasm. Cerebral blood flow (CBF) data have been useful in predicting the risk of vasospasm in these patients and in distinguishing those deficits caused by vasospasm. Although CBF thresholds for infarction have been established in animals, few clinical studies have correlated CBF values with neurological symptoms and infarction. To assess the sensitivity to ischemia provided by xenon-enhanced computed tomography (Xe/CT) of CBF and to define the clinical significance of specific values that it measures, we compared the clinical, CT, and Xe/CT findings on CBF in 51 patients with subarachnoid hemorrhage caused by ruptured aneurysms. Each patient had 1 to 6 Xe/CT studies. Fourteen patients had symptomatic vasospasm. In all 14, the first post deficit Xe/CT study found abruptly reduced CBF, either regionally or globally. In 9 of these 14 patients, flow values fell below 15 ml/100 g/min in 2 or more adjacent 2-cm cortical regions of interest, and in all 9, concurrent follow-up CT scans showed infarction in these regions. Eight of the 9 had paralysis and a severe sensory deficit. No patient whose CBF remained above 18 ml/100 g/min developed infarction. The blood flow studies caused neither significant complications nor neurological deterioration. The Xe/CT CBF method appears very sensitive to the early detection of symptomatic vasospasm. In most patients with subarachnoid hemorrhage, this noninvasive technique can replace angiography to delineate the location and severity of vasospasm, and may be useful in predicting the development of infarction.

scholarly journals TRAF3 mediates neuronal apoptosis in early brain injury following subarachnoid hemorrhage via targeting TAK1-dependent MAPKs and NF-κB pathways

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yan Zhou ◽  
Tao Tao ◽  
Guangjie Liu ◽  
Xuan Gao ◽  
Yongyue Gao ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Therapeutic Target ◽  
Cortical Neurons ◽  
Neuronal Apoptosis ◽  
Early Brain Injury ◽  
Neurological Deficits ◽  
Human Brain Tissue

AbstractNeuronal apoptosis has an important role in early brain injury (EBI) following subarachnoid hemorrhage (SAH). TRAF3 was reported as a promising therapeutic target for stroke management, which covered several neuronal apoptosis signaling cascades. Hence, the present study is aimed to determine whether downregulation of TRAF3 could be neuroprotective in SAH-induced EBI. An in vivo SAH model in mice was established by endovascular perforation. Meanwhile, primary cultured cortical neurons of mice treated with oxygen hemoglobin were applied to mimic SAH in vitro. Our results demonstrated that TRAF3 protein expression increased and expressed in neurons both in vivo and in vitro SAH models. TRAF3 siRNA reversed neuronal loss and improved neurological deficits in SAH mice, and reduced cell death in SAH primary neurons. Mechanistically, we found that TRAF3 directly binds to TAK1 and potentiates phosphorylation and activation of TAK1, which further enhances the activation of NF-κB and MAPKs pathways to induce neuronal apoptosis. Importantly, TRAF3 expression was elevated following SAH in human brain tissue and was mainly expressed in neurons. Taken together, our study demonstrates that TRAF3 is an upstream regulator of MAPKs and NF-κB pathways in SAH-induced EBI via its interaction with and activation of TAK1. Furthermore, the TRAF3 may serve as a novel therapeutic target in SAH-induced EBI.

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