Wijdicks, Eelco F. M.

Background and Purpose —The decision to proceed with surgery in cerebellar infarct with mass effect (CIMASS) in deteriorating patients is based on clinical features. The potential role of neuroimaging in predicting deterioration has not been systematically studied. In this study we determine the role of neuroimaging in predicting deterioration in CIMASS. Methods —We retrospectively reviewed the clinical and neuroimaging features in 90 patients with cerebellar infarcts. We selected for detailed analysis CIMASS in 35 patients. Results —Eighteen patients remained stable and 17 deteriorated. Of these 17 patients, 8 were treated conservatively and 9 had surgery. Radiological features indicative of progression were more common in deteriorating patients compared with stable patients: fourth ventricular shift (82.3% versus 50%, P =0.075, OR=4.67), hydrocephalus (76.5% versus 11.1%, P =0.0001, OR=26), brain stem deformity (47% versus 5.6%, P =0.0065, OR=15.1), and basal cistern compression (35.3% versus 0%, P =0.0076, OR=20.91). Differences in upward displacement of the aqueduct and pontomesencephalic junction from Twining’s line, tonsillar descent on sagittal MRI, and infarct volumes between stable and deteriorating patients were not statistically significant. Conclusions —Hydrocephalus, brain stem deformity, and basal cistern compression may herald deterioration in CIMASS. Admission to a neurological-neurosurgical intensive care unit and consideration of preemptive surgery are warranted in these patients. Vertical displacement of tonsils or aqueduct, demonstrated by MR imaging, did not predict deterioration.

Background and Purpose —The cause of pretruncal (perimesencephalic) nonaneurysmal subarachnoid hemorrhage is not known. MRI of the brain or spine is often performed to exclude any other vascular abnormalities. Its diagnostic value is not known. Methods —We used MR imaging of the brain with routine sequences, gadolinium enhancement, and additional thin T1-weighted axial sections following a triple dose of contrast. Results —We performed MR imaging of the brain in 18 patients with a pretruncal nonaneurysmal subarachnoid hemorrhage. The focal nature of the subarachnoid hemorrhage exclusively in front of the brain stem was confirmed in 14 patients studied within 7 days of the ictus. No vascular abnormalities were found in 17 cases, including 14 patients with gadolinium enhancement. An incidental capillary telangiectasia was found in 1 patient. Fluid-attenuated inverse recovery MR additionally documented blood in the sulci due to cerebrospinal fluid recirculation of blood. Five patients underwent MR imaging of the spine, and no arteriovenous malformations were found. Conclusions —MR imaging did not reveal a source of pretruncal subarachnoid hemorrhage. The cost of MR imaging probably outweighs the benefit in the evaluation of this variant of subarachnoid hemorrhage.

Background and Purpose Many patients with acute basilar artery occlusion may require endotracheal intubation and mechanical ventilation. The circumstances and predictive value for outcome in these patients are not well documented. Methods We reviewed the medical records of 25 patients admitted into the intensive care unit with a clinical diagnosis of acute basilar artery occlusion and need for mechanical ventilation. The medical records were reviewed for clinical features, breathing patterns, mode of mechanical ventilation, ability to wean from the ventilator, and neurological outcome. Results Apneic episodes resulted in endotracheal intubation in 8 patients. In the remaining 17 patients, intubation was needed for airway protection. Seven of 8 patients presenting with apneic episodes lost all brain stem reflexes. All 17 patients intubated for airway protection could be successfully weaned to a T-tube circuit. Outcome was generally poor and 22 patients died, of whom 7 died of early systemic complications. Only 3 of 25 patients, all with locked-in syndrome, survived. Conclusions Mortality is high in patients who require mechanical ventilation after acute basilar artery occlusion. No neurological improvement beyond a locked-in syndrome occurred in survivors. Recurrent apnea appears to predict further progression to brain stem death.

Nonaneurysmal perimesencephalic hemorrhage, a distinct form of subarachnoid hemorrhage, is a recently described variant of intracranial hemorrhage. We describe two patients who presented with unusual features of this type of subarachnoid hemorrhage and also two patients who had a perimesencephalic pattern of hemorrhage due to a ruptured posterior circulation aneurysm. The first patient, a 41-year-old woman with perimesencephalic hemorrhage, underwent an exploratory craniotomy because angiography had suggested an anomaly of the basilar tip. No source of hemorrhage could be identified at the time of surgery. The second patient was a 3-year-old boy who presented with opisthotonos and who was found to have a perimesencephalic hemorrhage. Angiography revealed no source for the hemorrhage. The third patient, a 54-year-old man, had a perimesencephalic pattern of subarachnoid hemorrhage from a vertebrobasilar junction aneurysm associated with a fenestration that was missed on the initial angiographic study. The fourth patient, a 43-year-old man, suffered a perimesencephalic pattern of subarachnoid hemorrhage from a small posterior cerebral artery aneurysm, which had not been recognized on two angiograms. These patients elaborate on the clinical spectrum of subarachnoid hemorrhage with a perimesencephalic pattern. First, a negative exploratory craniotomy suggests that the source of nonaneurysmal perimesencephalic hemorrhage may not be arterial. Second, nonaneurysmal perimesencephalic hemorrhage may also occur in children. Finally, the index of suspicion for a posterior circulation aneurysm should remain high in patients who present with a perimesencephalic pattern of subarachnoid hemorrhage, and these aneurysms may rise from unusual locations.

Patients with ischemic or hemorrhagic stroke are at risk for systemic complications. The reasons why gastrointestinal bleeding occurs after stroke are unknown and have intuitively been attributed to stress ulcers. No study to date has addressed causes of gastrointestinal hemorrhage in stroke. Between 1976 and 1994, 17 patients identified from the Mayo Clinic medical record system as having gastrointestinal hemorrhage and ischemic stroke (n = 14) or intracerebral hemorrhage (n = 3) were reviewed for presentation, associated causes, and outcome. Results of the endoscopic procedures were compiled, and available gastric biopsies were reviewed. In 17 patients with gastrointestinal bleeding after stroke, sudden hematemesis, a decrease in hemoglobin level, or orthostatic hypotension was found as a presenting feature. One patient presented with massive hematemesis, exsanguination, and cardiac arrest. Endoscopic findings were available in 14 patients and included gastroesophageal erosions, hemorrhagic gastritis, and gastric ulcer. In one patient, an adenocarcinoma of the gastric cardia was found. Putative pathogenetic agents were found in 16 of 17 patients and included a long history of nonsteroidal anti-inflammatory drugs (n = 6), acetylsalicylic acid (n = 3), grossly prolonged anticoagulation (n = 4), Helicobacter pylori (n = 2), and corticosteroids (n = 1). Gastrointestinal bleeding after stroke is rarely severe and may not contribute significantly to mortality. Medication-induced gastrointestinal hemorrhage may be underappreciated in this setting.

Intracerebral hematoma may complicate treatment of acute myocardial infarction in patients treated with fibrinolytic agents. We studied the clinical presentation and computed tomographic characteristics. We studied eight patients with lobar intracerebral hematomas after fibrinolytic treatment of acute coronary occlusion. All patients had electrocardiographic and laboratory evidence of acute myocardial infarction and were treated with tissue plasminogen activator or streptokinase followed by heparin infusion to prevent reocclusion. Computed tomography scans of 17 patients with cerebral hemorrhage from other causes were used for comparison. For most patients, outcome was fatal within hours of the ictus. Computed tomography scans showed superficially large lobar hematomas in six patients. One patient had a putaminal hemorrhage, and one had a vermis hemorrhage. Multiple sites of intracerebral hemorrhage were noted in three patients. Fluid levels inside the hematoma suggesting continuing hemorrhage into multiple compartments were common. Radiologically, fluid levels in hematomas, multiple hematomas, and blood in multiple compartments served to differentiate fibrinolysis-induced hemorrhage from hemorrhage of other causes. Severe amyloid angiopathy was found in one patient who was operated on. Hemorrhages in multiple compartments and the presence of fluid levels inside the hematoma suggest fibrinolysis-associated cerebral hematomas. Severe amyloid angiopathy may be a crucial factor in this clinical entity. Outcome is poor, and a high proportion of patients have rapid progression to brain death. Therefore, emergency neurosurgical evacuation will probably be unsuccessful.

Background and Purpose— There is uncertainty whether warfarin-treated patients (despite international normalized ratio <1.7) have increased risks of symptomatic intracerebral hemorrhage after intravenous thrombolysis. Methods— Vascular risk factors, stroke subtype, and outcome measures were compared between warfarin- and nonwarfarin-treated patients undergoing acute thrombolysis within 3 hours of symptom onset. Results— From 212 patients (mean age, 74±14 years; 50% men) studied, 14 (6.5%) had prior warfarin use. After adjusting for age, baseline National Institutes of Health Stroke Scale, and stroke subtype, warfarin-treated patients had significantly increased risks of developing symptomatic intracerebral hemorrhage (adjusted OR, 14.7; 95% CI, 1.3 to 54.3). A trend for poorer stroke recovery and increased mortality was observed in warfarin-treated patients on univariate, but not on multivariable, analyses. Conclusions— Warfarin-treated patients with stroke have increased risks of symptomatic intracerebral hemorrhage after thrombolytic treatment. These data raise safety concerns of thrombolytic treatment in warfarin-treated patients with subtherapeutic international normalized ratio.