Cerebral Infarction and Release of Platelet Thromboxane after Subarachnoid Hemorrhage

Neurosurgery ◽  
1990 ◽  
Vol 27 (6) ◽  
pp. 929-935 ◽  
Author(s):  
Seppo Juvela
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Infarction ◽  
Adenosine Diphosphate ◽  
Thromboxane B2 ◽  
Intracerebral Hematoma ◽  
Computed Tomographic ◽  
Computed Tomographic Scan ◽  
Aggregation Of Platelets ◽  
Platelet Thromboxane

Abstract Platelet aggregation induced by adenosine diphosphate and the release of thromboxane B2 were studied in 68 patients with subarachnoid hemorrhage during the second week after the hemorrhage, when delayed ischemic deterioration most often occurs. Follow-up computed tomographic scans were performed later than 1 month after subarachnoid hemorrhage to reveal permanent hypodense areas consistent with cerebral infarction. Occurrence of hypodense lesions on the follow-up computed tomographic scan was significantly associated with the presence of delayed ischemic deterioration (DID) (P<0.01). Patients with subcortical or cortical cerebral infarctions due to DID released more platelet thromboxane B2 than those with no evidence of a hypodense lesion on the computed tomographic scan (P<0.05). Hypodense areas caused by an intracerebral hematoma or small, deep-seated infarcts due to DID were not associated with significantly elevated release of thromboxane B2, but the lacunar type infarcts were associated with increased aggregation of platelets. The results suggest that augmented platelet function may be involved in the pathogenesis of cerebral infarction due to DID.

Nonsurgical Management of Spontaneous Intracerebral Hematoma

Neurosurgery ◽  
1981 ◽  
Vol 9 (4) ◽  
pp. 387-393 ◽  
Author(s):  
Thomas A. Duff ◽  
Sylovanius Ayeni ◽  
Allan B. Levin ◽  
Manucher Javid
Keyword(s):  
Continuous Monitoring ◽  
Perfusion Pressure ◽  
Primary Treatment ◽  
Intracerebral Hematoma ◽  
Statistical Comparison ◽  
Computed Tomographic ◽  
Nonsurgical Management ◽  
Computed Tomographic Scan ◽  
Admission Status

Abstract This report describes our experience with the use of osmotic diruetics, governed by continuous monitoring of intracranial pressure (ICP), as the primary treatment for 12 consecutive patients suffering from an acute, supratemtorial intracerebral hematoma. In all cases the hematoma, as shown by computed tomographic scan, had a long axis of >4.0 cm. ICP and cerebral perfusion pressure were successfully maintained within the assigned limits in all patients, and in none was surgical evacuation required. There was one death during the 6-month follow-up period. With appropriate weighting to differences in admission status, statistical comparison of the patient outcome in the present series with that reported by McKissock et al. suggests that ICP monitoring can improve the outcome of conservatively (and perhaps surgically) treated patients.

Recurrence of a Vertebral Artery Dissecting Pseudoaneurysm after Successful Stent-supported Coil Embolization: Case Report

Neurosurgery ◽  
2003 ◽  
Vol 53 (3) ◽  
pp. 754-761 ◽  
Author(s):  
Christopher I. MacKay ◽  
Patrick P. Han ◽  
Felipe C. Albuquerque ◽  
Cameron G. McDougall
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Neck Pain ◽  
Vertebral Artery ◽  
Coil Embolization ◽  
Artery Aneurysm ◽  
Left Vertebral Artery ◽  
Parent Vessel ◽  
Computed Tomographic ◽  
Computed Tomographic Scan

Abstract OBJECTIVE AND IMPORTANCE Dissecting aneurysms of the intracranial vertebral artery are increasingly recognized as a cause of subarachnoid hemorrhage. We present a case involving technical success of the stent-supported coil embolization but with recurrence of the dissecting pseudoaneurysm of the intracranial vertebral artery. The implications for the endovascular management of ruptured dissecting pseudoaneurysms of the intracranial vertebral artery are discussed. CLINICAL PRESENTATION A 36-year-old man with a remote history of head injury had recovered functionally to the point of independent living. He experienced the spontaneous onset of severe head and neck pain, which progressed rapidly to obtundation. A computed tomographic scan of the head revealed subarachnoid hemorrhage centered in the posterior fossa. The patient underwent cerebral angiography, which revealed dilation of the distal left vertebral artery consistent with a dissecting pseudoaneurysm. INTERVENTION Transfemoral access was achieved under general anesthesia, and two overlapping stents (3 mm in diameter and 14 mm long) were placed to cover the entire dissected segment. Follow-up angiography of the left vertebral artery showed the placement of the stents across the neck of the aneurysm; coil placement was satisfactory, with no residual aneurysm filling. Approximately 6 weeks after the patient's initial presentation, he developed the sudden onset of severe neck pain. A computed tomographic scan showed no subarachnoid hemorrhage, but computed tomographic angiography revealed that the previously treated left vertebral artery aneurysm had recurred. Angiography confirmed a recurrent pseudoaneurysm around the previously placed Guglielmi detachable coils. A test balloon occlusion was performed for 30 minutes. The patient's neurological examination was stable throughout the test occlusion period. Guglielmi detachable coil embolization of the left vertebral artery was then performed, sacrificing the artery at the level of the dissection. After the procedure was completed, no new neurological deficits occurred. On the second day after the procedure, the patient was discharged from the hospital. He was alert, oriented, and able to walk. CONCLUSION We appreciate the value of preserving a parent vessel when a dissecting pseudoaneurysm of the intracranial vertebral artery ruptures in patients with inadequate collateral blood flow, in patients with disease involving the contralateral vertebral artery, or in patients with both. However, our case represents a cautionary note that patients treated in this fashion require close clinical follow-up. We suggest that parent vessel occlusion be considered the first option for treatment in patients who will tolerate sacrifice of the parent vessel along its diseased segment. In the future, covered stent technology may resolve this dilemma for many of these patients.

Prevention of Rebleeding after Operation for Subarachnoid Hemorrhage of Unknown Cause

Neurosurgery ◽  
1985 ◽  
Vol 17 (6) ◽  
pp. 942-946 ◽  
Author(s):  
Noboru Sakai ◽  
Hiromu Yamada ◽  
Takashi Ando ◽  
Yasuaki Nishimura
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Surgical Treatment ◽  
Arterial Wall ◽  
Internal Carotid ◽  
Cerebral Arteries ◽  
Anterior Communicating Artery ◽  
Computed Tomographic ◽  
Follow Up Study ◽  
Computed Tomographic Scan

Abstract This study is presented to promote prophylactic operation to prevent rebleeding after subarachnoid hemorrhage (SAH) of unknown cause. Twenty-two cases of nontraumatic SAH of unknown cause of a total of 254 cases of SAH treated during a 5-year period (1980-1984) were available for this study. A follow-up study (4 to 61 months after treatment; median, 43 months) revealed a 4.5% mortality rate. Four patients chosen from among the 22 SAH cases underwent prophylactic operation. The decision to operate was based on repeated angiography showing regional cerebral vasospasm corresponding to a limited hyperdense area on the computed tomographic scan at the time of the onset of SAH. Microsurgery revealed a minute protrusion (less than 2 mm in diameter) or thinning of the arterial wall with old hematoma of the surrounding brain in all 4 cases, and treatment required only coating of the abnormal site. All 4 patients are now fully recovered. Frequently, abnormal changes of such cerebral arteries as the anterior communicating artery, the internal carotid artery (C-1 and C-2), and the middle cerebral artery (M-1) may occur. Therefore, the authors emphasize the necessity of surgical treatment for specific cases of SAH with an unknown cause.

scholarly journals The Computerized Tomographic Assessment of Brain Infarcts

1981 ◽  
Vol 8 (2) ◽  
pp. 121-126 ◽  
Author(s):  
D.E. Tubman ◽  
R. Ethier ◽  
D. Melançon ◽  
G. Bélanger ◽  
S. Taylor
Keyword(s):  
Cerebral Infarction ◽  
Clinical Diagnosis ◽  
Computed Tomographic ◽  
Brain Infarcts ◽  
Follow Up Studies

SUMMARY:The computed tomographic (CT) examinations of one hundred and sixty patients with a clinical diagnosis of cerebral infarction were reviewed. A characteristic CT pattern was noted. Infused scans and follow-up studies allowed for considerable accuracy in diagnosis.

Aspirin and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

1995 ◽  
Vol 82 (6) ◽  
pp. 945-952 ◽  
Author(s):  
Seppo Juvela
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Platelet Function ◽  
Delayed Cerebral Ischemia ◽  
Aneurysm Rupture ◽  
Content Type ◽  
Reduced Risk ◽  
Fine Print

✓ This follow-up study was designed to evaluate whether the use of aspirin either before or after aneurysm rupture affects the occurrence of delayed cerebral ischemia. Aspirin inhibits platelet function and thromboxane production and has been shown to reduce the risk of various cardiovascular and cerebrovascular ischemic diseases. Following admission, the patients in this study were interviewed regarding their use of aspirin and other medicines prior to and after hemorrhage, and their urine was screened qualitatively for salicylates. Patient outcome and the occurrence of hypodense lesions consistent with cerebral infarction on follow-up computerized tomography (CT) were studied prospectively up to 1 year after hemorrhage. Of 291 patients, 31 (11%) died because of the initial hemorrhage and 18 (6%) died due to rebleeding within 4 days after hemorrhage. Of the remaining 242 patients, 90 (37%) had delayed cerebral ischemia, which caused a permanent neurological deficit or death in 54 patients (22%). Of 195 patients undergoing follow-up CT, 85 (44%) had cerebral infarction that was not seen on the CT scan obtained on admission. Those who had salicylates in the urine on admission had a relative risk of 0.40 (95% confidence interval (CI), 0.15 to 1.10) of delayed ischemia with fixed deficit and a risk of 0.40 (95% CI, 0.18 to 0.93) of cerebral infarction compared with patients who did not have salicylates in their urine. This reduced risk of ischemic complications with aspirin use was restricted to those patients who used aspirin before hemorrhage, when the risk of ischemia was 0.21 (95% CI, 0.03 to 1.63) and the risk of infarct was 0.18 (95% CI, 0.04 to 0.84) compared with those who had not used aspirin. The reduced risk of cerebral infarction remained significant after adjustment for several potential confounding factors (adjusted risk 0.19; 95% CI, 0.04 to 0.89). These observations suggest that platelet function at the time of subarachnoid hemorrhage may be associated with delayed cerebral ischemia after aneurysm rupture.

scholarly journals Decompressive craniectomy in patients with cerebral infarction due to malignant vasospasm after aneurysmal subarachnoid hemorrhage

2012 ◽  
Vol 03 (03) ◽  
pp. 251-255 ◽  
Author(s):  
Saffet Tuzgen ◽  
Baris Kucukyuruk ◽  
Seckin Aydin ◽  
Fatma Ozlen ◽  
Osman Kizilkilic ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Infarction ◽  
Decompressive Craniectomy ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Clinical Results ◽  
Cerebral Infarct ◽  
World Federation ◽  
Life Saving

ABSTRACT Aim: The authors present their experience and the clinical results in decompressive craniectomy (DC) in patients with vasospasm after aneurysmal subarachnoid hemorrhage (SAH). Materials and Methods: Between 2002 and 2010, six patients underwent DC due to cerebral infarct and edema secondary to vasospasm after aneurysmal SAH. Four patients were male, and two were female. The age of patients ranged between 33 and 60 (mean: 47,6 ± 11,4). The follow up period ranged between 12 to 104 months (mean: 47,6 ± 36,6). The SAH grading according World Federation of Neurosurgeons (WFNS) score ranged between 3 to 5. Results: Last documented modified Rankin Score (mRS) ranged between 2 to 6. One patient died in the following year after decompression due to pneumonia and sepsis. Two patients had moderate disability (mRS of 4) and three patients continue their life with minimal deficit and no major dependency (mRS score 2 and 3). Conclusion: DC can be a life-saving procedure which provides a better outcome in patients with cerebral infarction secondary to vasospasm and SAH. However, the small number of the patients in this study is the main limitation of the accuracy of the results, and more studies with larger numbers are required to evaluate the efficiency of DC in this group of patients.

Timing of clinical grade assessment and poor outcome in patients with aneurysmal subarachnoid hemorrhage

2012 ◽  
Vol 117 (1) ◽  
pp. 15-19 ◽  
Author(s):  
Elias A. Giraldo ◽  
Jay N. Mandrekar ◽  
Mark N. Rubin ◽  
Stefan A. Dupont ◽  
Yi Zhang ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Infarction ◽  
Functional Outcome ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Intracerebral Hematoma ◽  
Poor Functional Outcome ◽  
Poor Outcome ◽  
Grade Assessment ◽  
Clinical Grading

Object Timing of clinical grading has not been fully studied in patients with aneurysmal subarachnoid hemorrhage (SAH). The primary objective of this study was to identify at which time point clinical assessment using the World Federation of Neurosurgical Societies (WFNS) grading scale and the Glasgow Coma Scale (GCS) is most predictive of poor functional outcome. Methods This study is a retrospective cohort study on the association between poor outcome and clinical grading determined at presentation, nadir, and postresuscitation. Poor functional outcome was defined as a Glasgow Outcome Scale score of 1–3 at 6 months after SAH. Results The authors identified 186 consecutive patients admitted to a teaching hospital between January 2002 and June 2008. The patients' mean age (± SD) was 56.9 ± 13.7 years, and 63% were women. Twenty-four percent had poor functional outcome (the mortality rate was 17%). On univariable logistic regression analyses, GCS score determined at presentation (OR 0.80, p < 0.0001), nadir (OR 0.73, p < 0.0001), and postresuscitation (OR 0.53, p < 0.0001); modified Fisher scale (OR 2.21, p = 0.0013); WFNS grade assessed at presentation (OR 1.92, p < 0.0001), nadir (OR 3.51, < 0.0001), and postresuscitation (OR 3.91, p < 0.0001); intracerebral hematoma on initial CT (OR 4.55, p < 0.0002); acute hydrocephalus (OR 2.29, p = 0.0375); and cerebral infarction (OR 4.84, p < 0.0001) were associated with poor outcome. On multivariable logistic regression analysis, only cerebral infarction (OR 5.80, p = 0.0013) and WFNS grade postresuscitation (OR 3.43, p < 0.0001) were associated with poor outcome. Receiver operating characteristic/area under the curve (AUC) analysis demonstrated that WFNS grade determined postresuscitation had a stronger association with poor outcome (AUC 0.90) than WFNS grade assessed upon admission or at nadir. Conclusions Timing of WFNS grade assessment affects its prognostic value. Outcome after aneurysmal SAH is best predicted by assessing WFNS grade after neurological resuscitation.

Hypertension as a Risk Factor for Epilepsy after Aneurysmal Subarachnoid Hemorrhage and Surgery

Neurosurgery ◽  
1990 ◽  
Vol 27 (4) ◽  
pp. 578-581 ◽  
Author(s):  
Juha öhman
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Epileptic Seizures ◽  
Consecutive Series ◽  
Computed Tomographic ◽  
Anticonvulsant Medication ◽  
Computed Tomographic Scan ◽  
History Of ◽  
The Difference ◽  
Lost To Follow Up

Abstract A prospective, consecutive series of 307 patients with aneurysmal subarachnoid hemorrhage ranging from Grades I to V according to the classification of Hunt and Hess on admission were evaluated to determine the incidence of epilepsy 1 to 3 years (mean, 1.4 years) after aneurysmal subarachnoid hemorrhage (SAH) and surgery. Sixty-three patients had died and one patient was lost to follow-up. Twenty-nine patients developed epileptic seizures after the SAH and surgery. The mean time from the SAH to epileptic seizure varied from 0 days (day of the SAH) to 2 years (mean, 6.7 months). The seizures were classified as focal in 9 patients (31%) and as generalized in 20 patients (69%). All patients received anticonvulsant medication after more than one seizure. The risk factors for development of posthemorrhagic/postoperative epilepsy were, in order of importance: a history of hypertension; an infarct on late computed tomographic scan; and the duration of coma after the ictus. Of the 85 patients with histories of hypertension, 17 (20.0%) developed epilepsy. Only 12 (5.4%) of the 222 nonhypertensive patients developed epileptic seizures. The difference between the groups was significant (P =0.0001). Computed tomographic scans were undertaken in 237 patients 1 to 3 years (mean, 1.4 years) after the SAH and surgery. Postoperative epilepsy was significantly associated with infarcts visualized on computed tomographic scan (P = 0.0005).

Sarcomatoid Carcinoma of the Gallbladder With a Rhabdoid Tumor Component

2003 ◽  
Vol 127 (10) ◽  
pp. e406-e408 ◽  
Author(s):  
Mi-Jung Kim ◽  
Eunsil Yu ◽  
Jae Y. Ro
Keyword(s):  
Sarcomatoid Carcinoma ◽  
Electron Microscopic Examination ◽  
Rhabdoid Tumor ◽  
Electron Microscopic ◽  
Mucin Production ◽  
Computed Tomographic ◽  
Rhabdoid Cells ◽  
Computed Tomographic Scan ◽  
History Of

Abstract We report the case of a sarcomatoid carcinoma with a rhabdoid tumor component originating in the gallbladder, along with immunohistochemical and electron microscopic findings. A 61-year-old woman presented with a 5-month history of right upper quadrant pain. Ultrasonography and a computed tomographic scan indicated gallbladder cancer. She underwent a cholecystectomy and a common bile duct resection. A firm mass (4.5 cm in greatest dimension) was present in the neck portion of the gallbladder. The mass was firm, solid, yellowish gray, and granular with areas of necrosis. Microscopically, the tumor was a biphasic sarcomatoid carcinoma and consisted of diffusely arranged pleomorphic cells, focally showing rhabdoid features and neoplastic glands with focal mucin production. Heterologous components such as osteoid, chondroid, and rhabdomyoblastic elements were not identified. By immunohistochemical staining, we demonstrated that the rhabdoid cells coexpressed cytokeratin and vimentin. On electron microscopic examination, the rhabdoid tumor cells showed cytoplasmic whorls of intermediate filaments in the cytoplasm and eccentric nuclei. Two months postoperatively, the follow-up computed tomographic scan showed multiple intrahepatic metastases and omental seedings.

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