Jimmy R. Fulgham

Predictors of Cerebral Infarction in Aneurysmal Subarachnoid Hemorrhage

Background— Clinical and radiologic predictors of cerebral infarction occurrence and location after aneurysmal subarachnoid hemorrhage have been seldom studied. Methods— We evaluated all patients admitted to our hospital with aneurysmal subarachnoid hemorrhage between 1998 and 2000. Cerebral infarction was defined as a new hypodensity located in a vascular distribution on computed tomography (CT) scan. Results— Fifty-seven of 143 patients (40%) developed a cerebral infarction. On univariate analysis, occurrence of cerebral infarction was associated with a worse World Federation of Neurological Surgeons grade (P =0.01), use of ventriculostomy catheter (P =0.01), preoperative vasospasm (P =0.03), surgical clipping (P =0.02), symptomatic vasospasm (P <0.01), and vasospasm on transcranial Doppler ultrasonography (TCD) or repeat angiogram (P <0.01). On multivariable analysis, only presence of symptoms ascribed to vasospasm (P <0.01) and evidence of vasospasm on TCD or angiogram predicted cerebral infarction (P <0.01). TCD and angiogram agreed on the diagnosis of vasospasm in 73% of cases (95% CI, 63% to 81%), but the diagnostic accuracy of this combination of tests was suboptimal for the prediction of cerebral infarction occurrence (sensitivity, 0.72; specificity, 0.68; positive predictive value, 0.67; negative predictive value, 0.72). Location of the cerebral infarction on delayed CT was predicted by neurological symptoms in 74%, by aneurysm location in 77%, and by angiographic vasospasm in 67%. Conclusions— Evidence of vasospasm on TCD and angiogram is predictive of cerebral infarction on CT scan but sensitivity and specificity are suboptimal. Cerebral infarction location cannot be predicted in one quarter to one third of patients by any of the studied clinical or radiological variables.

Intra-arterial Thrombolysis in Acute Basilar Artery Thromboembolism: The Initial Mayo Clinic Experience

OBJECTIVE To investigate the feasibility of intra-arterial thrombolysis in acute basilar artery thrombosis. DESIGN We reviewed a consecutive series of patients in whom intra-arterial thrombolysis was performed during the period from 1994 to 1996. MATERIAL AND METHODS Intra-arterial thrombolysis with urokinase was done in an attempt to recanalize the basilar artery in a series of nine patients with basilar artery thrombosis admitted to the neurologic intensive care unit. At the time of initial assessment, all nine patients had major neurologic deficits attributable to brain-stem ischemia, including two patients with locked-in syndrome. RESULTS Recanalization of the basilar artery system was successful in seven of the nine patients (a range of 2 to 13 hours after the ictus). Failure to recanalize the basilar artery occurred in two patients, who died after progressing to coma. Complete recovery or only minimal neurologic deficits were demonstrated in five of the nine patients. Despite recanalization of the basilar artery, two patients had no major change in their neurologic function, and both ultimately had severe ataxia and were fully dependent on others. A cerebellar hemorrhage occurred in one patient but without clinical worsening. Two patients had a retroperitoneal hematoma. CONCLUSION Intra-arterial thrombolysis with urokinase in acute basilar artery occlusion resulted in recanalization in seven of the nine patients (78%). Five of the nine patients recovered fully, including two patients who had had locked-in syndrome. In light of the devastating natural course of acute basilar artery occlusion, these initial results are encouraging and indicate that intra-arterial thrombolysis may be a useful emergency treatment, even in patients with prolonged symptoms of ischemia (up to 12 hours).

Subarachnoid hemorrhage: neurointensive care and aneurysm repair.

Aneurysmal subarachnoid hemorrhage (SAH) is often a neurologic catastrophe. Diagnosing SAH can be challenging, and treatment is complex, sophisticated, multidisciplinary, and rarely routine. This review emphasizes treatment in the intensive care unit, surgical and endovascular therapeutic options, and the current state of treatment of major complications such as cerebral vasospasm, acute hydrocephalus, and rebleeding. Outcome assessment in survivors of SAH and controversies in screening of family members are discussed.

Computed Tomographic Determinants of Neurologic Deterioration in Patients With Large Middle Cerebral Artery Infarctions

OBJECTIVE To identify specific radiographic features on computed tomographic (CT) imaging that can predict neurologic deterioration in patients with large middle cerebral artery (MCA) infarctions. PATIENTS AND METHODS We performed a 10-year retrospective review from January 1, 1991, through December 31, 2001, of medical records and CT scans of patients with large MCA infarctions. Neurologic deterioration was defied as progressive drowsiness or signs of herniation. The CT scans were grouped into 3 periods according to time after ictus. Radiographic features reviewed included hyperdense middle cerebral artery sign (HMCAS), more than a 50% loss of MCA territory, sulcal effacement, loss of lentiform nucleus or insular ribbon, and septal and pineal shift. Demographic and radiographic variables were compared by using t tests and the Fisher exact test. Prognostic values were calculated for all significant radiographic variables. RESULTS Thirty-four CT scans in 22 patients before neurologic deterioration were compared with 47 scans obtained in 14 patients without neurologic worsening. There were no demographic differences between groups. Initial analysis revealed that early (<12 hours) involvement of more than 50% of the MCA territory (P=.047; odds ratio [OR], 14.02; 95% confidence interval [CI], 1.04-189.42) and the HMCAS at any time (P<.001; OR, 21.6; 95% CI, 3.54-130.04) were independent predictors of neurologic deterioration. The positive predictive power for early involvement of more than 50% of the MCA and the HMCAS was 0.75 and 0.91, respectively. CONCLUSION The HMCAS and early CT evidence of more than 50% MCA involvement are predictive of neurologic deterioration in patients with large MCA infarcts.

Emerging medical and surgical management strategies in the evaluation and treatment of intracerebral hemorrhage

Intracerebral hemorrhage (ICH) accounts for approximately 10% of all strokes and causes high morbidity and mortality. Rupture of the small perforating vessels of the cerebral arteries is caused by chronic hypertension, which induces pathologic changes in the small vessels and accounts for most cases of ICH; however, amyloid angiopathy and other secondary causes are being seen more frequently with the increasing age of the population. Recent computed tomographic studies have revealed that ICH is a dynamic process with up to one third of initial hemorrhages expanding within the first several hours of ictus. Secondary injury is believed to result from the development of cerebral edema and the release of specific neurotoxins associated with the breakdown products of hemoglobin. Treatment is primarily supportive. Surgical evacuation is the treatment of choice for patients with neurologic deterioration from infratentorial hematomas. Randomized trials comparing surgical evacuation to medical management have shown no benefit of surgical removal of supratentorial hemorrhages. New strategies focusing on early hemostasis, improved critical care management, and less invasive surgical techniques for clot evacuation are promising to decrease secondary neurologic injury. We review the pathophysiology of ICH, its medical management, and new treatment strategies for improving patient outcome.

Meningoencephalitis Due to Blastomyces dermatitidis: Case Report and Literature Review

Infection of the central nervous system by Blastomyces dermatitidis is a rare cause of meningoencephalitis. The existence of exclusive clinical infection of the meninges in the absence of pulmonary or other foci of infection has been debated. We describe a 20-year-old man presenting with meningoencephalitis caused by B dermatitidis. Blastomycotic infection was confirmed by isolation of the organism from brain tissue obtained at biopsy. Magnetic resonance imaging demonstrated progressive enhancement of basal meninges with involvement of bilateral basal ganglia and thalami. Treatment with amphotericin B arrested further neurologic decline. However, clinical and radiographic follow-up suggested damage to diencephalic structures. The diagnosis of blastomycotic meningoencephalitis is difficult to establish because no sensitive serologic test exists, and attempts to isolate the organism in cerebrospinal fluid obtained by lumbar puncture generally fail. A biopsy specimen of brain tissue is frequently necessary for the diagnosis. Survival is possible with timely initiation of therapy.

Gastrointestinal bleeding in stroke.

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. Methods 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. Results 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). Conclusions Gastrointestinal bleeding after stroke is rarely severe and may not contribute significantly to mortality. Medication- induced gastrointestinal hemorrhage may be underappreciated in this setting.

Clinical Importance of Cardiac Troponin Release and Cardiac Abnormalities in Patients With Supratentorial Cerebral Hemorrhages

OBJECTIVE To determine the Incidence of cardiac troponin T (cTnT) elevation, electrocardiographic (ECG) changes, and arrhythmias in supratentorial intracerebral hemorrhage (ICH) and their association with early mortality. PATIENTS AND METHODS Patients with supratentorial ICHs admitted to Mayo Clinic, Rochester, Minn, from March 1998 to October 2003 were studied. We excluded moribund patients with ICHs who died within 12 hours of hospital admission. Cardiac troponin T levels measured on admission and day 2 were determined by a third-generation enzyme-linked immunosorbent assay. Continuous ECG monitoring was performed In all patients. Computed tomographic scans were graded and correlated with abnormal cardiac variables. RESULTS Peak levels of cTnT were elevated at 0.035 to 1.2 microg/L (mean +/- SD, 0.27 +/- 0.38 microg/L) in 10 (20%) of 49 patients and were not associated with changes in creatine kinase MB fraction or ECG results. The cTnT levels did not correlate with location or side of hemorrhage or mortality at 30 days. Seventy (64%) of 110 patients displayed ECG abnormalities. The ECG changes did not correlate with the location or side of ICH, hydrocephalus, midline shift, or extension to the ventricles. CONCLUSION The cTnT elevations in survivors of acute ICH are frequent but without confirmatory ECG changes that suggest mild myocardial injury. One-month mortality is not influenced by such cTnT elevations. In addition, ECG abnormalities are common but likely benign in patients with supratentorial ICH who survive the initial insult.

Rapidly progressive hippocampal atrophy: Evidence for a seizure-induced mechanism

Hippocampal formation atrophy (HFA) developed in an adult, who did not have epilepsy previously, after the occurrence of new-onset partial seizures from acute thrombosis of an ipsilateral parietal venous angioma. There was no evidence of hippocampal injury, and the patient had only one brief, generalized tonic-clonic seizure. Although HFA progressed rapidly over 5.5 months, the partial seizures did not become prolonged or secondarily generalized. Evidence from the patient indicates that partial seizure activity can cause rapid and progressive hippocampal atrophy.

Cerebral Venous Thrombosis Complicated by Hemorrhagic Infarction: Factors Affecting the Initiation and Safety of Anticoagulation

Background and Purpose: Anticoagulation (AC) may improve outcome in cerebral venous thrombosis (CVT), even when complicated by pretreatment hemorrhagic infarction (HI). The HI characteristics which affect the decision to initiate AC therapy and its outcome are unknown. We reviewed our experience with AC treatment for patients with CVT and HI. Methods: Retrospective study. Results: Two groups of patients were compared: those who received AC (n = 6) and those who did not (n = 6). Hemorrhage volumes ranged from petechial to large (93 cm3) hematoma with mass effect. Anticoagulated patients received treatment a mean of 11.3 days after symptom onset. Each had exclusively extratemporal HI without midline shift and had stable hemorrhage volumes and clinical status for at least 24 h prior to AC. AC did not increase HI volume or worsen clinical outcome. All 6 non-AC patients had enlarging hematomas. Four of these 6 patients had temporal HI; and two required hematoma resection. Conclusions: AC therapy was avoided in CVT patients with HI that were located in the temporal lobe, caused midline shift or were enlarging. AC was safely initiated within several days in clinically stable patients with non-temporal-lobe HI of unchanging volume. We suggest that the location and unchanged volume on serial CT may be important factors influencing the safety of AC therapy in patients with CVT and HI.