Hemorrhagic Transformation Rates following Contrast Media Administration in Patients Hospitalized with Ischemic Stroke.

BACKGROUND AND PURPOSE: Hemorrhagic transformation is a critical complication associated with ischemic stroke and has been associated with contrast media administration. The objective of our study was to use real-world in-hospital data to evaluate the correlation between contrast media type and transformation from ischemic to hemorrhagic stroke. MATERIALS AND METHODS: We obtained data on inpatient admissions with a diagnosis of ischemic stroke and a record of either iso-osmolar or low-osmolar iodinated contrast media for a stroke-related diagnostic test and a treatment procedure (thrombectomy, thrombolysis, or angioplasty). We performed multivariable regression analysis to assess the relationship between contrast media type and the development of hemorrhagic transformation during hospitalization, adjusting for patient characteristics, comorbid conditions, procedure type, a threshold for contrast media volume, and differences across hospitals. RESULTS: Inpatient visits with exclusive use of either low-osmolar (n = 38,130) or iso-osmolar contrast media (n = 4042) were included. We observed an overall risk reduction in hemorrhagic transformation among patients who received iso-osmolar compared with low-osmolar contrast media, with an absolute risk reduction of 1.4% (P = .032), relative risk reduction of 12.5%, and number needed to prevent harm of 70. This outcome was driven primarily by patients undergoing endovascular thrombectomy (n = 9211), in which iso-osmolar contrast media was associated with an absolute risk reduction of 4.6% (P = .028), a relative risk reduction of 20.8%, and number needed to prevent harm of 22, compared with low-osmolar contrast media. CONCLUSIONS: Iso-osmolar contrast media was associated with a lower rate of hemorrhagic transformation compared with low-osmolar contrast media in patients with ischemic stroke.

Spinal CSF-Venous Fistulas in Morbidly and Super Obese Patients with Spontaneous Intracranial Hypotension.

BACKGROUND AND PURPOSE: Spinal CSF-venous fistulas are increasingly recognized as the cause of spontaneous intracranial hypotension. Here, we describe the challenges in the care of patients with CSF-venous fistulas who are morbidly or super obese. MATERIALS AND METHODS: A review was undertaken of all patients with spontaneous intracranial hypotension and a body mass index of >40 who underwent digital subtraction myelography in the lateral decubitus position to look for CSF-venous fistulas. RESULTS: Eight patients with spontaneous intracranial hypotension with a body mass index of >40 underwent lateral decubitus digital subtraction myelography. The mean age of these 5 women and 3 men was 53 years (range, 45 to 68 years). Six patients were morbidly obese (body mass indexes = 40.2, 40.6, 41, 41.8, 45.4, and 46.9), and 2 were super obese (body mass indexes = 53.7 and 56.3). Lumbar puncture showed an elevated opening pressure in 5 patients (26.5-47 cm H2O). The combination of an elevated opening pressure and normal conventional spine imaging findings resulted in a misdiagnosis (midbrain glioma and demyelinating disease, respectively) in 2 patients. Prior treatment included surgical nerve root ligation for suspected CSF-venous fistula in 3 patients. Digital subtraction myelography demonstrated a CSF-venous fistula in 6 patients (75%). Rebound high-pressure headache occurred in all 6 patients following surgical ligation of the fistula, and papilledema developed in 3. CONCLUSIONS: In our series, opening pressure was generally elevated in patients with morbid or super obesity. The yield of identifying CSF-venous fistulas with digital subtraction myelography in this patient population can approach that of the nonobese patient population. These patients may be at higher risk of developing rebound high-pressure headaches and papilledema.

High Signal Intensity in the Dentate Nucleus and Globus Pallidus on Unenhanced T1-Weighted MR Images: Comparison between Gadobutrol and Linear Gadolinium-Based Contrast Agents.

BACKGROUND AND PURPOSE: In view of the recent observations that gadolinium deposits in brain tissue after intravenous injection, our aim of this study was to compare signal changes in the globus pallidus and dentate nucleus on unenhanced T1-weighted MR images in patients receiving serial doses of gadobutrol, a macrocyclic gadolinium-based contrast agent, with those seen in patients receiving linear gadolinium-based contrast agents. MATERIALS AND METHODS: This was a retrospective analysis of on-site patients with brain tumors. Fifty-nine patients received only gadobutrol, and 60 patients received only linear gadolinium-based contrast agents. Linear gadolinium-based contrast agents included gadoversetamide, gadobenate dimeglumine, and gadodiamide. T1 signal intensity in the globus pallidus, dentate nucleus, and pons was measured on the precontrast portions of patients' first and seventh brain MRIs. Ratios of signal intensity comparing the globus pallidus with the pons (globus pallidus/pons) and dentate nucleus with the pons (dentate nucleus/pons) were calculated. Changes in the above signal intensity ratios were compared within the gadobutrol and linear agent groups, as well as between groups. RESULTS: The dentate nucleus/pons signal ratio increased in the linear gadolinium-based contrast agent group (t = 4.215, P < .001), while no significant increase was seen in the gadobutrol group (t = -1.422, P = .08). The globus pallidus/pons ratios followed similarly, with an increase in the linear gadolinium-based contrast agent group (t = 2.931, P < .0001) and no significant change in those receiving gadobutrol (t = 0.684, P = .25). CONCLUSIONS: Successive doses of gadobutrol do not result in T1 shortening compared with changes seen in linear gadolinium-based contrast agents.

Diagnostic criteria for spontaneous spinal CSF leaks and intracranial hypotension.

BACKGROUND AND PURPOSE: Comprehensive diagnostic criteria encompassing the varied clinical and radiographic manifestations of spontaneous intracranial hypotension are not available. Therefore, we propose a new set of diagnostic criteria. MATERIALS AND METHODS: The diagnostic criteria are based on results of brain and spine imaging, clinical manifestations, results of lumbar puncture, and response to epidural blood patching. The diagnostic criteria include criterion A, the demonstration of extrathecal CSF on spinal imaging. If criterion A is not met, criterion B, which is cranial MR imaging findings of spontaneous intracranial hypotension, follows, with at least one of the following: 1) low opening pressure, 2) spinal meningeal diverticulum, or 3) improvement of symptoms after epidural blood patch. If criteria A and B are not met, there is criterion C, the presence of all of the following or at least 2 of the following if typical orthostatic headaches are present: 1) low opening pressure, 2) spinal meningeal diverticulum, and 3) improvement of symptoms after epidural blood patch. These criteria were applied to a group of 107 consecutive patients evaluated for spontaneous spinal CSF leaks and intracranial hypotension. RESULTS: The diagnosis was confirmed in 94 patients, with use of criterion A in 78 patients, criterion B in 11 patients, and criterion C in 5 patients. CONCLUSIONS: A new diagnostic scheme is presented reflecting the wide spectrum of clinical and radiographic manifestations of spontaneous spinal CSF leaks and intracranial hypotension.

Silent infarcts in children with sickle cell anemia and abnormal cerebral artery velocity.

BACKGROUND: A substantial minority of neurologically normal children with sickle cell disease have lesions consistent with cerebral infarction as seen on magnetic resonance imaging (MRI). OBJECTIVES: To determine if transfusion therapy affects the rate at which silent infarcts develop and to evaluate the contribution of MRI of the brain to stroke prediction by transcranial Doppler (TCD) ultrasonography. STUDY DESIGN: Children with elevated TCD ultrasonographic velocity were randomized to receive long-term transfusion therapy or standard care. Magnetic resonance imaging of the brain was obtained at randomization, annually, and with clinical neurologic events. The risk for new silent lesions and/or stroke was compared for each treatment arm. RESULTS: Among the 37% of subjects with silent infarcts, those receiving standard care were significantly more likely to develop new silent lesions or stroke than were those who received transfusion therapy. For subjects receiving standard care, those with lesions at baseline were significantly more likely to develop stroke or new silent lesions than those whose MRI studies showed no abnormality. CONCLUSIONS: Transfusion therapy lowers the risk for new silent infarct or stroke for children having both abnormal TCD ultrasonographic velocity and silent infarct. However, those with both abnormalities who are not provided transfusion therapy are at higher risk for developing a new silent infarct or stroke than are those whose initial MRI showed no abnormality. The finding of a silent infarct reinforces the need for TCD ultrasonographic screening and consideration of transfusion therapy if the abnormalities are seen. Similarly, elevated TCD ultrasonographic velocity warrants MRI of the brain because children with both abnormalities seem to be at increased risk for developing new silent infarct or stroke.

Silent infarction as a risk factor for overt stroke in children with sickle cell anemia: a report from the Cooperative Study of Sickle Cell Disease.

OBJECTIVE: To determine whether children with homozygous sickle cell anemia (SCD) who have silent infarcts on magnetic resonance imaging (MRI) of the brain are at increased risk for overt stroke. METHODS: We selected patients with homozygous SCD who (1) enrolled in the Cooperative Study of Sickle Cell Disease (CSSCD) before age 6 months, (2) had at least 1 study-mandated brain MRI at age 6 years or older, and (3) had no overt stroke before a first MRI. MRI results and clinical and laboratory parameters were tested as predictors of stroke. RESULTS: Among 248 eligible patients, mean age at first MRI was 8.3 +/- 1.9 years, and mean follow-up after baseline MRI was 5.2 +/- 2.2 years. Five (8.1%) of 62 patients with silent infarct had strokes compared with 1 (0.5%) of 186 patients without prior silent infarct; incidence per 100 patient-years of follow-up was increased 14-fold (1.45 per 100 patient-years vs 0.11 per 100 patient-years, P =.006). Of several clinical and laboratory parameters examined, silent infarct was the strongest independent predictor of stroke (hazard ratio = 7.2, P =.027). CONCLUSIONS: Silent infarct identified at age 6 years or older is associated with increased stroke risk.

Multicenter comparison of magnetic resonance imaging and transcranial Doppler ultrasonography in the evaluation of the central nervous system in children with sickle cell disease.

PURPOSE: To compare the results of standardized magnetic resonance imaging (MRI) of the brain and transcranial Doppler (TCD) ultrasonography of cerebral arteries in school-aged children with sickle cell disease to determine the correlation between these two different neurodiagnostic tests. PATIENTS AND METHODS: Data were analyzed from 78 children with sickle cell disease (mean age 11 yrs) who participated in both the Cooperative Study of Sickle Cell Disease (CSSCD) and the Stroke Prevention Trial in Sickle Cell Anemia (STOP). Patients who had experienced an overt stroke were excluded. MRI findings were classified as normal or "silent infarct." Results of TCD were classified as normal, conditional, or abnormal, based on the time-averaged maximum mean flow velocity in the proximal middle cerebral and distal internal carotid arteries. RESULTS: Of 61 patients who had a normal MRI examination, 11 (18%) had either conditional (5 patients) or abnormal (6 patients) TCD results. Among 17 patients in whom silent infarction was seen on MRI, only 5 (29%) had a conditional (1 patient) or abnormal (4 patients) TCD velocity. Thus, discordant results were seen in 23 patients: 12 in which the TCD result was normal and the MRI abnormal; 11 in which the TCD velocity was elevated and the MRI normal. CONCLUSIONS: Abnormal TCD and MRI examinations reveal different aspects of the pathophysiology of central nervous system (CNS) injury in sickle cell disease and are often discordant. Although TCD abnormality is predictive of overt stroke, the lack of concordance between TCD and MRI findings suggests a need to develop more sensitive and specific indicators of early CNS pathology, such as neuropsychometric testing and positron-emission tomography (PET) scans, and to obtain more information about microvascular pathologic processes that may affect CNS function.

Silent cerebral infarcts in sickle cell anemia: a risk factor analysis. The Cooperative Study of Sickle Cell Disease.

BACKGROUND: Silent infarcts have been reported in 17% of young patients with sickle cell disease and are associated with impaired performance on standardized psychometric tests. Risk factors for the development of these lesions have not been identified. METHODS: Investigators in the Cooperative Study of Sickle Cell Disease performed a brain magnetic resonance imaging scan on sickle cell anemia patients age 5.9 years and older who had been followed according to the protocols of the Cooperative Study since birth. Individuals with a known history of cerebrovascular accident were excluded from this analysis. Patients with and without silent infarctions were compared with regard to clinical and laboratory parameters. RESULTS: The study sample included 42 patients (18.3%) with silent infarcts. Patients who had silent infarcts were significantly more likely to have a clinical history of seizure and a lower painful event rate. Lower hemoglobin level, increased leukocyte count, elevated pocked red blood cell count, and SEN betaS globin gene haplotype were associated also with the presence of silent infarcts. There was no relationship between silent infarcts and platelet count, fetal hemoglobin level, reticulocyte percentage, serum aspartate aminotransferase level, total bilirubin concentration, blood pressure, growth parameters, or presence of alpha-thalassemia. A multivariate model for silent infarction identified the following as risk factors: low pain event rate, history of seizure, leukocyte count >/=11.8 x 10(9)/L, and the SEN betaS globin gene haplotype. CONCLUSIONS: Patients with risk factors for silent infarcts should be evaluated for cerebrovascular disease. If evidence of infarction is found, consideration must be given to therapeutic intervention. At present, the appropriate treatment has not been determined.

The spectrum of brain MR abnormalities in sickle-cell disease: a report from the Cooperative Study of Sickle Cell Disease.

PURPOSE: To define the spectrum of abnormalities in sickle-cell disease, including infarction, atrophy, and hemorrhage, that are identified by brain MR imaging. METHODS: All MR studies included T1, T2, and intermediate pulse sequences. Images were interpreted without knowledge of the clinical history or neurologic examination findings. Brain MR imaging was performed in 312 children with sickle-cell disease. RESULTS: Seventy patients (22%) had infarction/ischemia and/or atrophy, infarction/ischemia was noted in 39 children (13%) who had no history of a stroke (the "silent" group). The prevalence rates for silent lesions were 17% for sickle-cell anemia and 3% for hemoglobin sickle-cell disease. For patients with sickle-cell anemia and a history of cerebrovascular accident, infarction/ischemia lesions typically involved both cortex and deep white matter, while silent lesions usually were confined to deep white matter. Within the age range studied, the prevalence of infarction/ischemia did not increase significantly with age, although older patients with lesions had more lesions than did younger patients with lesions. CONCLUSIONS: Brain MR imaging showed infarction/ischemia in the absence of a recognized cerebrovascular accident in 13% of patients. The prevalence of these lesions did not increase significantly between the ages of 6 and 14 years, suggesting that lesions are present by age 6. However, the increase in the average number of lesions per patient with age may indicate progressive brain injury.

Resolution of pachymeningeal enhancement following dural puncture and blood patch.

We describe thickening and contrast enhancement of the intracranial pachymeninges, revealed by MRI in a patient with presumed low-pressure headache following dural puncture and a blood patch. The clinical and radiological abnormalities resolved within 2 weeks.

Ependymoma of the spinal nerve root: case report.

Ependymomas are the most common intramedullary tumor of the spinal cord. They are most common at the region of the cauda equina, accounting for up to 90% of primary tumors in that area. Extraspinal ependymomas are rare. We describe a case of an ependymoma arising in a spinal peripheral nerve root.

Embolization of the ophthalmic artery for control of epistaxis: report of two cases.

Embolization of the internal maxillary artery, an accepted method for control of severe or recurrent posterior epistaxis, usually involves the ipsilateral artery, but occasionally the contralateral vessel and the facial arteries as well. Such endovascular treatment may fail if the vascular supply to the bleeding vessels originates in derivative branches of the ophthalmic artery. We report two unusual cases in which embolization of the ophthalmic artery was performed to control epistaxis. The first patient had a prosthetic eye. In the second, sight in one eye was sacrificed after careful consideration in order to prolong life.

Cerebral infection complicating systemic aspergillosis in acute leukemia: clinical and radiographic presentation.

Cerebral fungal infection is becoming an increasingly recognized entity in immunocompromised patients on post-mortem examination. In order to determine the frequency of clinically significant cerebral fungal infection and define its clinical characteristics in a cohort of immunocompromised patients at high risk of fungal infection, the records of 118 patients with acute leukemia were examined for 57 clinical and laboratory features. The characteristics of 26 patients with systemic aspergillosis and acute leukemia were compared to 92 patients with acute leukemia in a control group. Eight of 118 patients (7%) had cerebral infection (seven Aspergillus, on Candida). Patients with systemic aspergillosis were more likely than patients in the control group to have focal neurologic findings (p = 0.02), confusion (p = 0.04), and abnormal computerized tomography (CT) of the brain characterized by single or multiple, enhancing or non-enhancing hypodense lesions (p = 0.02). Patients with systemic aspergillosis were more likely to die in complete remission than patients in the control group (p = 0.003); three of six patients with aspergillosis who died in remission expired as a consequence of cerebral infection. Cerebral infection complicated systemic Aspergillus infection in seven of 26 patients (27%), versus one of 16 patients with systemic Candida infection (6%) (p = NS). The authors conclude, therefore, that systemic aspergillosis complicating acute leukemia is more likely to be associated with confusion, focal neurologic findings, and abnormal CT scan of the brain, and that these findings suggest the presence of cerebral infection. In addition, cerebral infection commonly complicates the course of systemic aspergillosis, and is a significant cause of morbidity and mortality in patients with acute leukemia. A high index of suspicion is needed to insure early diagnosis and appropriate therapy, particularly in those who achieve remission of their leukemia.

Primary central nervous system lymphoma in acquired immune deficiency syndrome. A clinical and pathologic study with results of treatment with radiation.

Primary central nervous system (CNS) lymphoma occurs frequently in patients with the acquired immune deficiency syndrome (AIDS). Seventeen patients with AIDS and biopsy-proven CNS lymphoma were treated with whole-brain radiation. At presentation, most patients were severely debilitated from previous AIDS-related illnesses. Patients generally had focal neurologic symptoms such as seizures and paralysis. Headaches and mental status changes, often noticed after hospital admission, seldom brought our patients to seek medical attention. Computed tomography (CT) scan showed low-density, contrast-enhancing, mass lesions with variable amounts of peritumor edema. Size, location, and pattern of contrast enhancement of the lesions varied. No specific pattern was seen that could be used to distinguish between CNS lymphoma, toxoplasmosis, or other CNS diseases that occur in patients with AIDS. Biopsy results showed angiocentric, high-grade, large cell tumors with frequent necrosis. Immunohistochemical analysis showed B-cell phenotype with small amounts of T-cells, presumably reactive. All patients received irradiation to the whole brain with parallel opposed fields. A variety of doses and treatment regimens were used. Mean survival was only 72 days. Survival was longer in patients with higher pretreatment Karnofsky scores. The correlation between dose and survival was not significant. At completion of therapy, most patients showed improvement in Karnofsky score and had partial improvement in neurologic symptoms. CNS lymphomas in patients with AIDS are responsive to radiation. Posttreatment CT scans showed regression of tumors. Autopsy examinations showed regression of tumors, but also showed concurrent CNS infections, AIDS encephalopathy, and radiation-induced changes within the normal CNS tissue. Opportunistic infections rather than cerebral herniation or uncontrolled lymphoma was the most common cause of death.

Incidental paranasal sinus abnormalities on MRI of the brain.

T2-weighted magnetic resonance imaging (MRI) presents paranasal sinus pathology with remarkable clarity. However, it has yet to be demonstrated that all MRI findings represent true pathology and not minor or incidental findings of no consequence. In an effort to resolve this question, we have analysed retrospectively 263 consecutive T2-weighted MRI examinations of the head performed for indications not associated with possible sinus pathology. We examined these studies for abnormally increased signal in the paranasal sinuses and the sites of involvement. Mucoperiosteal thickening, mucus retention cysts, air-fluid levels or total sinus opacification were recorded. Of the 263 studies examined, 65 (24.7%) demonstrated abnormalities in the paranasal sinuses. We conclude that because of its great sensitivity MRI will often detect abnormalities in the paranasal sinuses which are unrelated to the patients' presenting problems.

CT appearance of primary CNS lymphoma in patients with acquired immunodeficiency syndrome.

Cranial CT studies of 32 patients with biopsy-proven AIDS-related primary CNS lymphoma were reviewed retrospectively. A wide variety of different CT appearances were identified. Mass lesions varied in location, size, and number. Most lesions were either iso- or hyperdense and all enhanced with contrast medium. Several different patterns of enhancement were observed. Mass effect and edema were seen in almost all patients. After radiotherapy, most tumors decreased in diameter, became hypodense, and no longer enhanced with contrast medium. Edema and mass effect decreased or resolved in all but one patient. Postradiotherapy CT scans also revealed interval enlargement of the ventricles and cortical sulci. This study demonstrates the wide diversity of CT appearances of AIDS-related primary CNS lymphoma. The CT findings cannot be used in lieu of biopsy for diagnosis of this disorder. The appearance of postradiotherapy CT scans was consistent with regressing lymphoma.

Progressive visual field defects in patients with intracranial arteriovenous malformations.

Two men, aged 59 and 36 years, had large, intracranial arteriovenous malformations. Both patients developed severe, bilateral visual loss secondary to unrecognized chronic papilledema. Lumbar puncture disclosed increased intracranial pressure. Neuroimaging disclosed only vascular malformations. The patients were treated by embolization of the vascular malformations and ventriculoperitoneal shunting procedures. The malformation of one patient was excised.