US nationwide trends in carotid revascularization: hospital outcome and predictors of outcome from 1998 to 2007.

OBJECTIVES: The goals of the study were to assess US nationwide trends in hospital outcome following carotid endarterectomy (CEA) and carotid angioplasty and stenting (CAS) and to determine potential predictors of outcome. METHODS: The Nationwide Inpatient Sample, constituting a 20% representative and stratified sample of non-federal US hospitals, was analyzed retrospectively from years 1998 to 2007. RESULTS: The annual number of CEA decreased (137,877-111,658) and increased for CAS (2318-14,415). Inhospital mortality following CEA decreased from 0.4% to 0.3% (P < 0.001), whereas long-term facility (LTF) discharge increased from 8.2% to 10.5% (P < 0.001). Discharge outcome improved for CAS in both categories (mortality 2-0.5%; LTF discharge 10.7-8.3%; both P < 0.001). The trend analysis revealed an increase in patient age and a worsening comorbid profile over time. Age, women, length of stay, atrial fibrillation, and carotid stenosis with infarction were important determinants of unfavorable hospital outcome. CONCLUSION: From a nationwide practice perspective, the number of carotid revascularizations fell by 10%. CEA has resulted in stable hospital mortality rates. Meanwhile, CAS has been increasingly utilized with overall improvement in short-term outcome. Our results further suggest a decrease in the number of patients with treatment-eligible carotid disease over time. However, the increasing prevalence of high-risk comorbidity in the aging population may pose a challenge to revascularization strategies.

US nationwide trends in carotid revascularization: is there a clinical opportunity cost associated with the introduction of novel medical devices?

OBJECTIVES: Nationwide practice patterns during the implementation of novel technology, such as carotid angioplasty and stenting (CAS) and embolic protection devices (EPD), and the clinical impact thereof have received less attention. METHODS: The Nationwide Inpatient Sample, constituting a 20% representative sample of non-federal US hospitals, was analyzed from years 1998 to 2007. Hospital outcome was stratified into in-hospital mortality (IHM), long-term facility discharge, and home/ short-term facility discharge (HSF). RESULTS: Discharge outcome improved for CAS over the decade. However, this improvement occurred in two phases with a period of worsening (2003-2005) in between. During this transition period, the risk of IHM following CAS was increased (RR 1.29-2.43) and was lower for good outcome (HSF: RR 0.97-0.99) when compared with 2002/2003. During the same transition period, carotid endarterectomy (CEA) was associated with a lower risk of IHM (RR 0.75-1.00), but also a lower risk of HSF (RR 0.98-0.99). CONCLUSIONS: The results lead to the hypothesis that the nationwide introduction of CAS-EPD may have been associated with temporary increases in in-hospital mortality and discharge morbidity. If such 'clinical opportunity costs' exist with the widespread introduction and adoption of new medical technology with proven efficacy in randomized trials, effective mechanisms are needed for mitigation or prevention during the transition period.

Diagnosis and treatment of arteriovenous malformations.

Brain arteriovenous malformations (bAVMs) are among the least common of causes of brain hemorrhage, seizures, or headaches. Embedded in the brain, their widely varying size, arterial feeders draining venous pattern and nidus complexity make them among the most challenging of disorders for attempted eradication. The low prevalence has created a literature long dominated by anecdote, only recently and slowly being clarified by epidemiological, pathophysiological, and imaging data. A first-ever randomized clinical trial seeks to determine if invasive intervention to eradicate the lesion--and its attendant risks of complications--offers a better prognosis than awaiting a hemorrhage before undertaking such efforts.

Dysplastic vessels after surgery for brain arteriovenous malformations.

BACKGROUND AND PURPOSE: The cause and clinical significance of residual dysplastic vessels after surgery for brain arteriovenous malformations (AVM) are unclear. We studied predictors and frequency of residual dysplastic vessels on cerebral angiography after AVM surgery. METHODS: The 240 prospectively enrolled surgical patients from the New York AVM Databank underwent 269 AVM-related surgical procedures. Reported postoperative brain angiographic findings were classified post hoc as showing (1) persistent dysplastic vessels, (2) a residual AVM, (3) focal hyperemia in the surgical bed, (4) other changes, or (5) a normal angiogram. Univariate and multivariate models were applied to test for an association between residual dysplastic vessels and patient age, sex, preoperative AVM size, anatomic AVM location, number of embolization procedures before surgery, and the time interval between AVM surgery and the postoperative angiogram. RESULTS: Of the 224 documented postoperative angiograms, 78 (35%) showed dysplastic vessels, 24 (11%) had evidence for a residual AVM, 16 (7%) showed focal hyperemia, 6 (2%) revealed other findings, and 100 (45%) were normal. The number of cases showing angiographic evidence for dysplastic vessels was significantly associated with increasing size of the AVM (in millimeter increments; P=0.0001); the mean diameter of AVMs in patients showing dysplastic vessels after surgery was significantly larger (41 mm, SD +/-14) than in those without residual dysplastic vessels (27 mm, SD +/-13; P<0.001). Symptomatic postoperative intracerebral hemorrhage occurred in 4 patients (1%), in 2 of whom dysplastic vessels were seen on the postoperative angiogram. CONCLUSIONS: The findings suggest that persistent dysplastic vessels may be found in approximately one third of angiograms after AVM surgery. Preoperative AVM size was found to be an independent predictor for the occurrence of dysplastic vessels on the postoperative angiogram.

Association of infratentorial brain arteriovenous malformations with hemorrhage at initial presentation.

BACKGROUND AND PURPOSE: The goal of this study was to analyze the association of hemorrhagic presentation with infratentorial brain arteriovenous malformations (AVMs). METHODS: The 623 consecutive, prospectively enrolled patients from the Columbia AVM Databank were analyzed in a cross-sectional study. Clinical presentation (diagnostic event) was categorized as intracranial hemorrhage or nonhemorrhagic presentation. From brain imaging and cerebral angiography, AVM location was classified as either infratentorial or supratentorial. Univariate and multivariate statistical models were applied to test the effect of age, sex, AVM size and location, venous drainage pattern, and associated (ie, feeding artery or intranidal) arterial aneurysms on the likelihood of hemorrhage at initial AVM presentation. RESULTS: Of the 623 patients, 72 (12%) had an infratentorial and 551 (88%) had a supratentorial AVM. Intracranial hemorrhage was the presenting symptom in 283 patients (45%), and infratentorial AVM location was significantly more frequent (18%) among patients who bled initially (6%; odds ratio [OR], 3.60; 95% confidence interval [CI], 2.09 to 6.20). This difference remained significant (OR, 1.99; 95% CI, 1.07 to 3.69) in the multivariate logistic regression model controlling for age, sex, AVM size, deep venous drainage, and associated arterial aneurysms. In the same model, the effect of other established determinants for AVM hemorrhage--ie, AVM size (in 1-mm increments; OR, 0.95; 95% CI, 0.94 to 0.96), deep venous drainage (OR, 3.09; 95% CI, 1.87 to 5.12), and associated aneurysms (OR, 2.78; 95% CI, 1.76 to 4.40)--remained significant. CONCLUSIONS: Our findings suggest that infratentorial AVM location is independently associated with hemorrhagic AVM presentation.

The New York Islands AVM Study: design, study progress, and initial results.

BACKGROUND AND PURPOSE: Prospective population-based data on the incidence of brain arteriovenous malformation (AVM) hemorrhage are scarce. We studied lifetime detection rates of brain AVM and incident AVM hemorrhage in a defined population. METHODS: The New York islands (ie, Manhattan Island, Staten Island, and Long Island) comprise a 9,429,541 population according to the 2000 census. Since March 15, 2000, all major New York islands hospitals have prospectively reported data on consecutive patients living in the study area with a diagnosis of brain AVM and whether the patient had suffered AVM hemorrhage. Patients living outside the ZIP code-defined study area were excluded from the study population. RESULTS: As of June 14, 2002, 284 prospective AVM patients (mean+/-SD age, 35+/-18 years; 49% women) were encountered during 21,216,467 person-years of observation, leading to an average annual AVM detection rate of 1.34 per 100,000 person-years (95% CI, 1.18 to 1.49). The incidence of first-ever AVM hemorrhage (n=108; mean age, 31+/-19 years; 45% women) was 0.51 per 100,000 person-years (95% CI, 0.41 to 0.61). The estimated prevalence of AVM hemorrhage among detected cases (n=144; mean age, 33+/-19 years; 50% women) was 0.68 per 100,000 (95% CI, 0.57 to 0.79). CONCLUSIONS: Our prospective data, spanning 27 months, suggest stable rates for AVM detection and incident AVM hemorrhage. Approximately half of AVM patients may suffer intracranial hemorrhage.

Effect of age on clinical and morphological characteristics in patients with brain arteriovenous malformation.

BACKGROUND AND PURPOSE: The goal of this work was to determine the effect of age at initial presentation on clinical and morphological characteristics in patients with brain arteriovenous malformation (AVM). METHODS: The 542 consecutive patients from the prospective Columbia AVM database (mean+/-SD age, 34+/-15 years) were analyzed. Univariate statistical models were used to test the effect of age at initial presentation on clinical (AVM hemorrhage, seizures, headaches, neurological deficit, other/asymptomatic) and morphological (AVM size, venous drainage pattern, AVM brain location, concurrent arterial aneurysms) characteristics. RESULTS: Hemorrhage was the presenting symptom in 46% (n=247); 29% (n=155) presented with seizures, 13% (n=71) with headaches, 7% (n=36) with a neurological deficit, and 6% (n=33) without AVM-related symptoms. Increasing age correlated positively with intracranial hemorrhage (P=0.001), focal neurological deficits (P=0.007), infratentorial AVMs (P<0.001), and concurrent arterial aneurysms (P<0.001); an inverse correlation was found with seizures (P<0.001), AVM size (P=0.001), and lobar (P<0.001), deep (P=0.008), and borderzone (P=0.014) location. No age differences were found for sex, headache, asymptomatic presentation, and venous drainage pattern. CONCLUSIONS: Our data suggest a significant interaction of patient age and clinical and morphological AVM features and argue against uniform AVM characteristics across different age classes at initial presentation. In particular, AVM patients diagnosed at a higher age show a higher fraction of AVM hemorrhage and are more likely to harbor additional risk factors such as concurrent arterial aneurysms and small AVM diameter. Longitudinal population-based AVM data are necessary to confirm these findings.

Incident hemorrhage risk of brain arteriovenous malformations located in the arterial borderzones.

BACKGROUND AND PURPOSE: We sought to assess the relative risk of hemorrhagic presentation of brain arteriovenous malformations (AVMs) located in the arterial borderzone territories. METHODS: The 464 consecutive, prospectively enrolled patients from the New York AVM Databank were analyzed. AVM borderzone location was coded positive when the malformation was supplied by branches of at least 2 of the major circle of Willis arteries (anterior, middle, and/or posterior cerebral arteries). AVMs fed by branches of only 1 major pial or any other single artery served as a comparison group. Clinical presentation (diagnostic event) was categorized as (1) intracranial hemorrhage, proven by brain imaging, or (2) seizure, focal neurological deficit, headache, or other event with no signs of AVM hemorrhage on brain imaging. RESULTS: In 48% (n=222) of the patients, AVMs were located in the arterial borderzone territories; in 52% (n=242) a non-borderzone location was found. Hemorrhage was the presenting symptom in 44% (n=205); 28% (n=132) presented with seizures, 11% (n=52) with headaches, 7% (n=34) with a neurological deficit, and 9% (n=41) with other or no AVM-related symptoms. The frequency of incident AVM hemorrhage was significantly lower in borderzone AVMs (27%, n=61) than in non-borderzone malformations (60%, n=144; P:<0.001). This difference remained significant in a multivariate model controlling for age, sex, AVM size, deep venous drainage, and presence of aneurysms (odds ratio, 0.4; 95% CI, 0.25 to 0.66). CONCLUSIONS: Our findings suggest that borderzone location is an independent determinant for a lower risk of AVM hemorrhage at initial presentation.

Risk of endovascular treatment of brain arteriovenous malformations.

BACKGROUND AND PURPOSE: Independently assessed data on frequency, severity, and determinants of neurological deficits after endovascular treatment of brain arteriovenous malformations (AVMs) are scarce. METHODS: From the prospective Columbia AVM Study Project, 233 consecutive patients with brain AVM receiving > or =1 endovascular treatments were analyzed. Neurological impairment was assessed by a neurologist using the Rankin Scale before and after completed endovascular therapy. Multivariate logistic regression models were used to identify demographic, clinical, and morphological predictors of treatment-related neurological deficits. The analysis included the components used in the Spetzler-Martin risk score for AVM surgery (AVM size, venous drainage pattern, and eloquence of AVM location). RESULTS: The 233 patients were treated with 545 endovascular procedures. Mean follow-up time was 9.6 months (SD, 18.1 months). Two hundred patients (86%) experienced no change in neurological status after treatment, and 33 patients (14%) showed treatment-related neurological deficits. Of the latter, 5 (2%) had persistent disabling deficits (Rankin score >2), and 2 (1%) died. Increasing patient age [odds ratio (OR), 1.04; 95% confidence interval (CI), 1.01 to 1.08], number of embolizations (OR, 1.41; 95% CI, 1.16 to 1.70), and absence of a pretreatment neurological deficit (OR, 4.55; 95% CI, 1.03 to 20.0) were associated with new neurological deficits. None of the morphological AVM characteristics tested predicted treatment complications. CONCLUSIONS: From independent neurological assessment and prospective data collection, our findings suggest a low rate of disabling treatment complications in this center for endovascular brain AVM treatment. Risk predictors for endovascular treatment differ from those for AVM surgery.

A theoretical model of cerebral hemodynamics: application to the study of arteriovenous malformations.

A comprehensive computer model of the cerebral circulation, based on both hydrodynamics and electrical network analysis, was used to investigate the influences of arteriovenous malformations (AVM) on regional cerebral hemodynamics. The basic model contained 114 normal compartments: 55 arteries, 37 veins, 20 microvessel groups (MVG), one compartment representing systemic and extracranial vascular resistance, and one representing the heart. Each microvessel group, which represented the arteriolar bed, consisted of 5000 microvessels. Cerebral blood flow autoregulation was simulated by a formula that determined the resistance and therefore the flow rate of the microvessel groups (arterioles) as a function of perfusion pressure. Elasticity was introduced to describe the compliance of each vessel. Flow rate was made a controlling factor for the positive regulation of the diameters of conductance vessels by calculation of shear stress on the vessel wall (vessel dilation). Models containing an AVM were constructed by adding an AVM compartment and its feeding arteries and draining veins. In addition to the basic model, AVM models were simulated with and without autoregulation and flow-induced conductance vessel dilation to evaluate the contributions of these factors on cerebral hemodynamics. Results for the model with vessel dilation were more similar to clinical observations than those without vessel dilation. Even in the presence of total vasoparalysis of the arteriolar bed equivalent, obliteration of a large (1000 mL/min) shunt flow AVM resulted in a near-field CBF increase from a baseline of 21 to a post-occlusion value of no more than 74 mL/100 g/min, casting doubt on a purely hemodynamic basis for severe hyperemia after treatment. The results of the simulations suggest that our model may be a useful tool to study hemodynamic problems of the cerebral circulation.

Developmental deficits in adult patients with arteriovenous malformations.

BACKGROUND: Cerebral arteriovenous malformations (AVMs) are congenital masses of arteries and veins that appear to undergo an unclear "maturation" for many years. Using structured interviews, we compared developmental history of adult patients with AVM with a comparison group of patients with cerebral tumor or aneurysm. OBJECTIVE: To determine whether a remote history of developmental abnormality in adult patients with AVM might be an early marker of cerebral status. DESIGN: Adult patients with AVM and a comparison group of patients with cerebral aneurysm or low-grade tumor participated in a survey. SETTING: Urban medical school-based tertiary care center. PATIENTS: Forty-four randomly selected patients with AVM from the Columbia-Presbyterian AVM Database. There were 32 comparison patients:15 randomly chosen patients from the institution's Cerebral Aneurysm Database and all 17 patients who underwent a biopsy from 1990 to 1995 with a diagnosis of low-grade tumor and who could be contacted. MAIN OUTCOME MEASURES: A brief, structured interview adapted from the Centers for Disease Control and Prevention for its 1994 study of the prevalence of learning disabilities in American children. We defined the positive occurrence of a condition as an affirmative answer to the question, " Did have (condition) during his/her school-age years?" Each patient was also asked if there had been any problems in the following skill areas: reading, writing, listening, speaking, attention, impulsivity, organization, mathematics, or drawing. The AVM size was calculated on the angiographic film by measuring its longest diameter in any dimension. RESULTS: Patients with AVM were significantly more likely to report a positive occurrence to any survey question (P<.05). Two thirds of all patients with AVM (66%) reported at least 1 skill difficulty during their school years, significantly more than the comparison group (P<.001). Neither the maximum AVM diameter nor the occurrence of hemorrhage as an adult differed between patients with AVM with and without early skill difficulty. CONCLUSIONS: Patients with AVM are more likely to report a developmental learning disorder than patients with tumor or aneurysm despite the absence of other neurologic symptoms of diseases not diagnosed for another 20 years. These data support the notion that disorders of behavioral and intellectual function are sensitive markers of early cerebral status.

The experience of Wernicke's aphasia.

The authors induced a transient Wernicke's aphasia in a patient with left frontal arteriovenous malformation by superselective Wada injection exclusively into the lower division of the left middle cerebral artery. The patient was then asked to recall his experience, which the authors matched against his language during anesthesia. The patient's account showed that there was a more systematic attempt to respond appropriately than the authors could infer from his overt behavior. His narrative suggests that a thought process not measured by aphasia examinations may exist independent of language.

Anterior translocation of language in patients with left cerebral arteriovenous malformation.

We studied seven patients with left cerebral atriovenous malformation (AVM) with superselective arterial injection of anesthetics during angiography to determine whether there was translocation of some language functions to other regions in the ispilateral hemisphere. All patients were right handed. With a catheter inserted into each target vessel, patients underwent aphasia examination in an A-B-A design: (A) baseline, no anesthetic; (B) 1 minute after anesthetic injection; and (A) 12 minutes after injection (when its effects had dissipated). The results showed that six of seven patients had no significant aphasia at baseline or 12 minutes after anesthetic injection. One patient had a mild conduction aphasia at baseline and after anesthetic effects had dissipated. In the six patients with temporoparietal AVM, anesthetic injections into vessels in the lower division of the middle cerebral artery (MCA) not feeding the AVM (e.g., the left angular artery) produced a wide range of language function--from conduction aphasia to dense Wernicke's syndromes. When upper division MCA vessels were injected (e.g., the prefrontal branch), all developed a major aphasic disorder with significant comprehension defects. A seventh patient with a frontal opercular AVM had a mild anomia, semantic paraphasias, and decreased word-list generation when the prefrontal branch was injected. Her comprehension, however, was intact. These data show that patients with posterior cerebral AVM can show language abnormalities where such deficits are not typically seen after acute brain injury. These findings support a posterior-to-anterior extension of some language skills under conditions of brain disease.

Intraoperative monitoring of motor evoked potentials: a review of 116 cases.

We reviewed the results of motor evoked potential (MEP) and somatosensory evoked potential (SEP) monitoring during 116 operations on the spine or spinal cord. We monitored MEPs by electrically stimulating the spinal cord and recording compound muscle action potentials from lower extremity muscles and monitored SEPs by stimulating posterior tibial or peroneal nerves and recording both cortical and subcortical evoked potentials. We maintained anesthesia with an N2O/O2/opioid technique supplemented with a halogenated inhalational agent and maintained partial neuromuscular blockade using a vecuronium infusion. Both MEPs and SEPs could be recorded in 99 cases (85%). Neither MEPs nor SEPs were recorded in eight patients, all of whom had preexisting severe myelopathies. Only SEPs could be recorded in two patients, and only MEPs were obtained in seven cases. Deterioration of evoked potentials occurred during nine operations (8%). In eight cases, both SEPs and MEPs deteriorated; in one case, only MEPs deteriorated. In four cases, the changes in the monitored signals led to major alterations in the surgery. We believe that optimal monitoring during spinal surgery requires recording both SEPs and MEPs. This provides independent verification of spinal cord integrity using two parallel but independent systems, and also allows detection of the occasional insults that selectively affect either motor or sensory systems.

Interhemispheric transfer of language in patients with left frontal cerebral arteriovenous malformation.

Cerebral arteriovenous malformations (AVMs) are frequently evaluated before therapeutic embolization by superselective injection of anesthetics into individual arterial branches so as to determine whether permanent occlusion would affect eloquent function. In Experiment 1, we used this adaptation of the Wada procedure to study three right-handed adult patients with left frontal cerebral AVMs by injecting vessels in Wernicke's and Broca's areas, respectively, and assessing language functions. The results showed that superselective testing in the inferior division of the left MCA in all three patients produced a dense Wernicke's aphasia. Injections into the left frontal regions, however, resulted in right paresis in all patients, but no language deficits including no loss of fluency. In Experiment 2, Patient 2 underwent fMRI activation for spontaneous word-list generation using multi-slice echo planar BOLD techniques at 1.5 Tesla. A voxel-by-voxel comparison of rest vs activation for each task was performed with a Z-score threshold of 2.5 SD for activated voxels. There was activation in the right hemisphere in the insula, frontal operculum pars opercularis, and inferior frontal gyrus, an area homologous to Broca's area in the left hemisphere. There was also activation in the left hemisphere in the Rolandic region, but language function was unaffected during Wada testing in this area. These data suggested that features of expressive language were no longer controlled by the left frontal lobe where the AVM was located, and provided new evidence for interhemispheric re-organization under conditions of chronic neurovascular disease.

Cerebral SPECT imaging: effect on clinical management.

This study, performed in 94 consecutive patients referred for evaluation, demonstrates the clinical utility of cerebral SPECT imaging. In a significant percentage of patients (47%), the additional information provided by SPECT resulted in an alteration in clinical management. Long-term follow-up will be necessary to determine the effect of these management decisions on patient outcome.

Can induction of systemic hypotension help prevent nidus rupture complicating arteriovenous malformation embolization?: analysis of underlying mechanism achieved using a theoretical model.

BACKGROUND AND PURPOSE: Nidus rupture is a serious complication of intracranial arteriovenous malformation (AVM) embolotherapy, but its pathogenetic mechanisms are not well described. An AVM model based on electrical network analysis was used to investigate theoretically the potential role of hemodynamic perturbations for elevating the risk of nidus vessel rupture (Rrupt) after simulated AVM embolotherapy, and to assess the potential benefit of systemic hypotension for preventing rupture. METHODS: Five separate hypothetical mechanisms for nidus hemorrhage were studied: 1) intranidal rerouting of blood pressure; 2) extranidal rerouting of blood pressure; 3) occlusion of draining veins with glue; 4) delayed thrombosis of draining veins; and 5) excessively high injection pressures proximal to the nidus. Simulated occlusion of vessels or elevated injection pressures were implemented into the AVM model, and electrical circuit analysis revealed the consequent changes in intranidal flow, pressure, and Rrupt for the nidus vessels. An expression for Rrupt was derived based on the functional distribution of the critical radii of component vessels. If AVM rupture was observed (Rrupt > or = 100%) at systemic normotension (mean pressure [P] = 74 mm Hg), the theoretical embolization was repeated under systemic hypotension (minor P = 70 mm Hg, moderate P = 50 mm Hg, or profound P = 25 mm Hg) to assess the potential benefit of this maneuver in reducing hemorrhage rates. RESULTS: All five pathogenetic mechanisms under investigation were able to produce rupture of AVMs during or after embolotherapy. These different mechanisms had in common the capability of generating surges in intranidal hemodynamic parameters resulting in nidus vessel rupture. The theoretical induction of systemic hypotension during and after treatment was shown to be of significant benefit in attenuating these surges and reducing Rrupt to safer levels below 100%. CONCLUSION: The induction of systemic hypotension during and after AVM embolization would appear theoretically to be of potential use in preventing iatrogenic nidus hemorrhage. The described AVM model should serve as a useful research tool for further theoretical investigations of AVM embolotherapy and its hemodynamic sequelae.

Experimental in vivo imaging of the cranial perineural lymphatic pathway.

After intraventricular injection of 99mTc antimony sulfide in rabbits (n = 12) and cats (n = 14), radiolabeled colloid was imaged passing into the nasal mucosa and subsequently into the cervical lymph nodes. The cervical lymph nodes accounted for about 12% of the injected dose in rabbits sacrificed at 22-24 hr after injection and about 5% of the injected dose in cats sacrificed at 5-6 hr after injection. In both animals this represented at least one-third of the cerebrospinal fluid colloid clearance. This technique is applicable to in vivo imaging studies of the perineural lymphatic pathway for cerebrospinal fluid absorption in primates and, with modifications, in human subjects.

The detection of intracranial calcifications by MR.

Twenty patients in whom CT had unequivocally demonstrated the presence of calcification in a diversity of lesions and who had undergone MR, performed at 0.6 T and with standard T1- and T2-weighted pulse sequences, were retrospectively studied to determine the MR signal-intensity characteristics of the calcifications and to assess the ability of MR to detect the presence of this abnormality. CT proved superior to MR in detecting and characterizing calcification. In seven of 20 cases, the apparent extent of calcification was equal by both imaging techniques, and in 13 of the 20 cases, CT showed more extensive abnormality. In five of the 20 cases, the calcifications were seen by MR as regions of profoundly reduced signal intensity, approximately equal to cortical bone, in all pulse sequences. In 12 of the 20 cases, the signal intensity was profoundly reduced in one or more, but not all, pulse sequences. T2-weighted pulse sequences were most sensitive in detecting calcification of signal void. Reviewed without knowledge of the CT findings, the MR images were interpreted as definitely indicative of the presence of calcification in three of the 20 cases. In seven of the 20 cases, the MR images raised the possibility of calcification but were less definitive than the CT findings. In 10 of the 20 cases, MR was judged indeterminate for the presence of calcification.