Early onset of PRES in a patient with a subarachnoid haemorrhage due to a ruptured intracranial aneurysm.

Posterior reversible encephalopathy syndrome (PRES) is rarely associated with subarachnoid haemorrhage (SAH). We present a case involving a patient who developed PRES, prior to induction of hypertensive therapy, 2 days after the onset of a SAH due to a ruptured intracranial aneurysm.

Quantitative assessment of cerebral hemodynamics using perfusion-weighted MRI in patients with major cerebral artery occlusive disease: comparison with positron emission tomography.

BACKGROUND AND PURPOSE: Cerebrovascular reactivity (CVR) to acetazolamide is a key parameter in determining the severity of hemodynamic impairment in patients with major cerebral artery occlusive disease. Perfusion-weighted MRI (PW MRI) can measure the cerebral blood volume (CBV) as an indicator of hemodynamic impairment. CBV measured by PW MRI was compared with CVR measured by positron emission tomography (PET). METHODS: Twelve normal subjects and 17 patients with major cerebral artery occlusive disease underwent PW MRI and PET. The images were coregistered with 3-dimensional spoiled gradient-recalled acquisition images. Quantitative PW MRI-CBV maps were generated using the indicator dilution method with arterial input function. One large cortical region of interest for each unilateral middle cerebral artery territory was determined on each image. PET-CVR was calculated by measuring cerebral blood flow before and after acetazolamide challenge. RESULTS: A significant negative correlation was observed between PW MRI-CBV and PET-CVR (r=-0.713; P<0.0001). PW MRI-CBV higher than the mean +2 SD obtained in normal subjects (15.2 mL/100 g) was defined as elevated and PET-CVR lower than the mean -2 SD obtained in normal subjects (15.1%) was defined as reduced. Assuming the PET-CVR as the true determinant of hemodynamic impairment, PW MRI-CBV provided 80.0% sensitivity and 91.7% specificity, with 80.0% positive predictive value for detecting patients with reduced CVR. CONCLUSIONS: The PW MRI-CBV method can simply and accurately identify patients with hemodynamic impairment without exposure to ionizing radiation.

Postoperative cerebral hyperperfusion associated with impaired cognitive function in patients undergoing carotid endarterectomy.

OBJECT: Cognitive impairment occurs in 20 to 30% of patients following carotid endarterectomy (CEA). The purpose of the present study was to determine whether postoperative cerebral hyperperfusion is associated with impairment of cognitive function in patients undergoing that procedure. METHODS: Cerebral blood flow (CBF) was measured using single-photon emission computerized tomography scanning before and immediately after CEA and on the 3rd postoperative day in 92 patients with ipsilateral internal carotid artery stenosis of 70% or greater. Hyperperfusion post-CEA was defined as a 100% increase or greater in CBF compared with preoperative values. Neuropsychological testing was also performed preoperatively and at the 1-, 3-, and 6-month follow-up examinations. At the 1-month postoperative neuropsychological assessment, 11 patients (12%) displayed evidence of cognitive impairment. In addition, the incidence of postoperative cognitive impairment in patients with post-CEA hype perfusion (seven [58%] of 12 patients) was significantly higher than that in patients without post-CEA hyperperfusion (four [5%] of 80 patients; p < 0.0001). A logistic regression analysis demonstrated that post-CEA hyperperfusion was the only significant independent predictor of postoperative cognitive impairment. Of the seven patients in whom post-CEA hyperperfusion and cognitive impairment were identified 1 month postoperatively, four (including three patients with hyperperfusion syndrome) remained cognitively impaired at the 3- and 6-month follow-up examinations. CONCLUSIONS: Postoperative cerebral hyperperfusion is associated with impairment of cognitive function in patients undergoing CEA. Furthermore, the development of hyperperfusion syndrome is associated with the persistence of postoperative cognitive impairment.

Effects of the free radical scavenger, edaravone, on the development of postoperative cognitive impairment in patients undergoing carotid endarterectomy.

BACKGROUND: Some patients undergoing carotid endarterectomy (CEA) experience postoperative cognitive impairment. The purpose of the present case cohort study with historical control was to determine whether pretreatment with a novel free radical scavenger, edaravone, could prevent development of cognitive impairment after CEA. METHODS: Fifty-five patients with ipsilateral internal carotid artery (ICA) stenosis (> or =70%) underwent CEA with administration of edaravone before ICA clamping. Neuropsychological testing was performed preoperatively and at the first postoperative month. Cerebral blood flow was also measured using single-photon emission computed tomography before and immediately after CEA and on the third postoperative day. RESULTS: Postoperative cognitive impairment was observed in only 1 (2%) patient, who exhibited postoperative cerebral hyperperfusion (cerebral blood flow increase > or =100% compared with preoperative values). Incidence of postoperative cognitive impairment in the control group (92 CEA patients without administration of edaravone) was significantly higher (12%) (P = .0298, control vs treatment group). Logistic regression analysis demonstrated that postoperative cerebral hyperperfusion and absence of pretreatment with edaravone were significant independent predictors of postoperative cognitive impairment. CONCLUSION: Pretreatment with edaravone can prevent development of cognitive impairment after CEA.

Ruptured vertebral artery dissecting aneurysm followed by spontaneous acute occlusion and early recanalization: case report.

A 47-year-old man presented with a ruptured vertebral artery dissecting aneurysm manifesting as subarachnoid hemorrhage followed by acute occlusion and early recanalization of the affected artery. Cerebral angiography 2 hours after the onset of the symptom showed pearl-and-string sign in the right vertebral artery. Serial angiography showed that the affected artery was occluded at 12 hours but was recanalized on the 4th day. The dissecting aneurysm was resected with side-to-side anastomosis between the bilateral posterior inferior cerebellar arteries. Postoperative cerebral angiography demonstrated disappearance of the lesion and patency of the right posterior inferior cerebellar artery via the anastomosis. Histological examination of the lesion showed hematoma between the media and adventitia, disrupting the internal elastica and intima. Acute occlusion and early recanalization of the affected artery may occur in ruptured vertebral artery dissecting aneurysms. Serial neurological and neuroradiological examinations are essential to decide the timing and method of treatment.

Transcranial regional cerebral oxygen saturation monitoring during carotid endarterectomy as a predictor of postoperative hyperperfusion.

OBJECTIVE: Hyperperfusion syndrome is a rare but potentially devastating complication that can occur after carotid endarterectomy (CEA). The purpose of this study was to determine whether intraoperative transcranial regional cerebral oxygen saturation (rSO(2)) monitoring via near-infrared spectroscopy could be reliably used to identify patients at risk for post-CEA hyperperfusion. METHODS: rSO(2) was intraoperatively monitored for 50 patients undergoing CEA for treatment of ipsilateral internal carotid artery stenosis (>/=70%). Cerebral blood flow (CBF) was also assessed, with single-photon emission computed tomography, before and immediately after CEA. RESULTS: Post-CEA hyperperfusion (CBF increase of >/=100%, compared with preoperative values) was observed for six patients. A significant linear correlation was observed between the rSO(2) increases immediately after declamping of the internal carotid artery and the CBF increases immediately after CEA (r(2) = 0.247, P = 0.0002). The sensitivity and specificity of the rSO(2) increases for detection of post-CEA hyperperfusion were 100 and 86.4%, respectively, with a cutoff point of 5%. A strong linear correlation was observed between the rSO(2) increases at the end of the procedure and the CBF increases immediately after CEA (r(2) = 0.822, P < 0.0001). Both the sensitivity and the specificity of the rSO(2) increases for detection of post-CEA hyperperfusion were 100% with a cutoff point of 10%. Hyperperfusion syndrome developed for one patient with post-CEA hyperperfusion, but intracerebral hemorrhage did not occur. CONCLUSION: Intraoperative rSO(2) monitoring can reliably identify patients at risk for hyperperfusion after CEA.

Intracerebral hemorrhage after carotid endarterectomy associated with asymptomatic perioperative cerebral ischemia detected by cerebral perfusion imaging: case report.

BACKGROUND: Risk factors for intracerebral hemorrhage following carotid endarterectomy (CEA) include perioperative cerebral ischemia, postoperative cerebral hyperperfusion, and postoperative anticoagulation therapy, and at least 2 of these risk factors are typically present in the context of intracerebral hemorrhage (ICH). CASE DESCRIPTION: A 75-year-old man with severe bilateral cervical internal carotid artery stenosis and a minor stroke resulting in left motor weakness underwent a right CEA. The operation was uneventful, and the patient did not experience new neurologic deficits upon recovery from anesthesia. Brain single photon emission computed tomography (SPECT) obtained immediately after CEA showed a perfusion defect in the right parietal lobe and absence of cerebral hyperperfusion. A computed tomography (CT) scan showed no new abnormal findings. Aspirin therapy was instituted postoperatively. On the second postoperative day, the patient experienced abrupt worsening of left hemiparesis, and subsequent CT imaging demonstrated a hematoma in the right parietal lobe. Cerebral hyperperfusion was absent on repeat SPECT. CONCLUSION: Perioperative cerebral ischemia can result in intracerebral hemorrhage after CEA even in the absence of cerebral hyperperfusion and/or anticoagulation therapy. Further, cerebral perfusion imaging performed immediately after CEA is a useful modality for the identification of occult cerebral ischemia or hyperperfusion that may lead to intracerebral hemorrhage.

Hemorrhagic gastric and duodenal ulcers after the Great East Japan Earthquake Disaster.

AIM: To elucidate the characteristics of hemorrhagic gastric/duodenal ulcers in a post-earthquake period within one medical district. METHODS: Hemorrhagic gastric/duodenal ulcers in the Iwate Prefectural Kamaishi Hospital during the 6-mo period after the Great East Japan Earthquake Disaster were reviewed retrospectively. The subjects were 27 patients who visited our hospital with a chief complaint of hematemesis or hemorrhagic stool and were diagnosed as having hemorrhagic gastric/duodenal ulcers by upper gastrointestinal endoscopy during a 6-mo period starting on March 11, 2011. This period was divided into two phases: the acute stress phase, comprising the first month after the earthquake disaster, and the chronic stress phase, from the second through the sixth month. The following items were analyzed according to these phases: age, sex, sites and number of ulcers, peptic ulcer history, status of Helicobacter pylori (H. pylori) infection, intake of non-steroidal anti-inflammatory drugs, and degree of impact of the earthquake disaster. RESULTS: In the acute stress phase from 10 d to 1 mo after the disaster, the number of patients increased rapidly, with a nearly equal male-to-female ratio, and the rate of multiple ulcers was significantly higher than in the previous year (88.9% vs 25%, P < 0.005). In the chronic stress phase starting 1 mo after the earthquake disaster, the number of patients decreased to a level similar to that of the previous year. There were more male patients during this period, and many patients tended to have a solitary ulcer. All patients with duodenal ulcers found in the acute stress phase were negative for serum H. pylori antibodies, and this was significantly different from the previous year's positive rate of 75% (P < 0.05). CONCLUSION: Severe stress caused by an earthquake disaster may have affected the characteristics of hemorrhagic gastric/duodenal ulcers.

Pretreatment with the free radical scavenger edaravone prevents cerebral hyperperfusion after carotid endarterectomy.

OBJECTIVE: Cerebral hyperperfusion syndrome after carotid endarterectomy (CEA) is a rare but potentially devastating complication. The purpose of the present study, which was not a randomized controlled trial but a case cohort study with historical control, was to determine whether pretreatment with a novel free radical scavenger, edaravone, could prevent occurrence of cerebral hyperperfusion after CEA. METHODS: Fifty patients with ipsilateral internal carotid artery stenosis (>/=70%) underwent CEA with administration of edaravone before internal carotid artery clamping. Preoperative cerebral blood flow and cerebrovascular reactivity (CVR) to acetazolamide were assessed with single-photon emission computed tomography (SPECT). Cerebral blood flow also was measured immediately after CEA and on the 3rd postoperative day. RESULTS: Cerebral hyperperfusion (cerebral blood flow increase >/=100% compared with preoperative values) was revealed by SPECT performed immediately after CEA in only one patient (2%), who also exhibited reduced preoperative CVR. The incidence of post-CEA hyperperfusion as revealed by SPECT in the control group (51 CEA patients without administration of edaravone) was significantly higher (16%) (P = 0.0310, control versus treatment group). In addition, in a subgroup of patients with reduced preoperative CVR, the incidence of post-CEA hyperperfusion as revealed by SPECT in the edaravone group (7%) was significantly lower than that in the control group (67%) (P = 0.0029). Logistic regression analysis demonstrated that reduced preoperative CVR and absence of pretreatment with edaravone were significant independent predictors of post-CEA hyperperfusion as revealed by SPECT. CONCLUSION: Pretreatment with edaravone can prevent occurrence of cerebral hyperperfusion after CEA.