Significance of hyperintense vessels on FLAIR MRI in acute stroke.

OBJECTIVE: To describe hyperintense vessels sign (HVS) in patients with acute stroke on fluid-attenuated inversion recovery (FLAIR) MRI and determine its clinical significance and utility. BACKGROUND: Enhancement of vessels on postcontrast MRI in patients with acute stroke is considered an indicator of early brain ischemia. Recently, the FLAIR technique has shown promise in earlier and better detection of ischemic brain parenchymal lesions. METHODS: Two observers retrospectively reviewed 304 MRI of patients with stroke and identified 30 patients with acute middle cerebral artery stroke and HVS on FLAIR obtained within 24 hours of symptom onset. These patients were evaluated with contrast-enhanced MRI (n = 9), MR angiography of carotid and intracranial circulation (n = 30), cerebral angiography (n = 8), transcranial Doppler (n = 17), and SPECT (n = 16). The extent of HVS was compared with final infarct size and NIH Stroke Scale score. RESULTS: HVS on FLAIR was seen in 10% of the patients with acute stroke. HVS was associated with large vessel occlusion or severe stenosis (>90%). Intravascular enhancement on contrast MRI was observed in vessels that were hyperintense on FLAIR. Both cortical and subcortical infarcts demonstrated HVS. MR angiographic and cerebral angiographic findings of large vessel occlusion or severe stenosis (>90%), slow flow, low velocities by transcranial Doppler, and hypoperfusion on SPECT correlated with HVS. HVS was the earliest ischemic change in three patients scanned within 3 hours of ictus. Final infarct size was smaller than the area showing HVS in all patients. CONCLUSION: HVS on FLAIR MRI is an indicator of slow flow and early ischemia as a result of large vessel occlusion or stenosis and inadequacy of collateral circulation. HVS does not mean that infarction has occurred but indicates brain tissue at risk of infarction. It should prompt consideration of revascularization and flow augmentation strategies.

MRI in cerebral intraventricular hemorrhage: analysis of 50 consecutive cases.

MRI of intraventricular haemorrhage (IVH) has not been studied formally. We aimed to describe the degradation rate and patterns shown on 1.5 T MRI in IVH, comparing them to other coexisting brain hemorrhage. We studied 50 consecutive cases using T1-, proton-density, and T2-weighted images. IVH was seen in two forms: layered (free-flowing in ventricles) (37 cases) and/or clotted (31). Both were best shown by proton-density image. Layered IVH was seen in the dependent portions of the lateral ventricles with fluid ("blood-CSF") levels, degrading more slowly than both clotted IVH and intraparenchymal hemorrhages (IPH) (acute blood products persisting for several more days; P < 0.05). Clotted IVH degraded at a rate comparable to IPH. IVH cleared rapidly and did not form hemosiderin. Subarachnoid hemorrhage (SAH) cleared faster and was less conspicuous than IVH. Hypertensive (22), aneurysmal (11), traumatic (2), idiopathic (9), or vascular malformation-related (6) IVH were seen. IVH coexisted with IPH (30) or SAH (12), or both (12). The high rate of layering with blood-CSF levels in IVH is most likely due to different densities of blood components and CSF and the fibrinolytic capability of the latter. Delayed degradation of layered IVH probably reflects high intraventricular oxygen and glucose content. Further study is necessary to determine if MRI characteristics of IVH are helpful in excluding other intraventricular diseases such as neoplasia and pyocephalus.

MRI findings in lumbar puncture headache syndrome: abnormal dural-meningeal and dural venous sinus enhancement.

Intracranial hypotension (IH) is a treatable cause of persistent headaches. Persistent cerebrospinal fluid (CSF) leak at a lumbar puncture (LP) site may cause IH. We present postcontrast MRI of a patient with post-lumbar-puncture headache (LPHA) showing abnormal, intense, diffuse, symmetric, contiguous dural-meningeal (pachymeningeal) enhancement of the supratentorial and infratentorial intracranial dura, including convexities, interhemispheric fissure, tentorium, and falx. MRI also showed abnormal dural venous sinus enhancement, a new finding in LPHA, suggesting compensatory venous expansion. Thus, IH and venodilatation may play a role in the development of LPHA.

Fluid-attenuated inversion-recovery MR imaging in acute and subacute cerebral intraventricular hemorrhage.

BACKGROUND AND PURPOSE: Fluid-attenuated inversion-recovery (FLAIR) MR imaging may show subarachnoid hemorrhage (SAH) with high sensitivity. We hypothesized that the FLAIR technique is effective and reliable in the diagnosis of cerebral intraventricular hemorrhage (IVH). METHODS: Two observers evaluated the 1.5-T MR fast spin-echo FLAIR images, T1- and T2-weighted MR images, and CT scans of 13 patients with IVH and the FLAIR images of 40 control subjects. RESULTS: IVH appeared bright on the FLAIR images obtained during the first 48 hours and was of variable appearance at later stages. FLAIR MR imaging detected 12 of 13 cases of IVH; no control subjects were falsely thought to have IVH (92% sensitivity, 100% specificity). However, IVH could not be fully excluded in the third ventricle (20%, n = 8) or in the fourth ventricle (28%, n = 11) on some control images because of CSF pulsation artifacts. Two cases had CT-negative IVH seen on FLAIR images. One case had FLAIR-negative IVH seen by CT. Although the sensitivities of conventional MR imaging (92%) and CT (85%) were also high, FLAIR imaging showed IVH more conspicuously than did standard MR imaging and CT in 62% of the cases (n = 8). FLAIR was as good as or better than CT in showing IVH in 10 cases (77%). FLAIR images showed all coexisting SAH. CONCLUSION: FLAIR MR imaging identifies acute and subacute IVH in the lateral ventricles with high sensitivity and specificity. In cases of subacute IVH, conventional MR imaging complements FLAIR in detecting IVH. The usefulness of the FLAIR technique for detecting third and fourth ventricular IVH may be compromised by artifacts. Blood hemoglobin degradation most likely causes the variable FLAIR appearance of IVH after the first 48 hours.

Aggressive giant pituitary adenoma presenting as a nasopharyngeal mass: magnetic resonance imaging and pathologic findings.

We report a giant pituitary adenoma with aggressive histologic features that prominently invaded the nasopharynx. Magnetic resonance imaging (MRI) demonstrated a large heterogeneous nodular mass that was hypointense to isointense on T1-weighted images and mixed hypointense, isointense, and hyperintense on T2-weighted images. The mass measured 7.5 x 5 x 7 cm, extending from the nasopharynx posteriorly through the clivus, and superiorly through the paranasal sinuses, and sellar-suprasellar region. After contrast administration, heterogeneous nodular enhancement was noted. A nasopharyngeal neoplasm extending into the sella was suspected because voice change and nasal speech long preceded the patient's visual symptoms. A biopsy disclosed an aggressive, infiltrating, hemorrhagic tumor, which was diagnosed as a non-secreting pituitary macroadenoma. This report indicates that pituitary adenomas may grow invasively to tremendously large sizes resulting in their initial presentation as nasopharyngeal masses.

Cranial magnetic resonance imaging findings in bacterial endocarditis: the neuroimaging spectrum of septic brain embolization demonstrated in twelve patients.

Infective endocarditis (IE) is an elusive systemic disorder that is often associated with neurologic complications. The contribution of brain magnetic resonance imaging (MRI) to the diagnosis of IE and the spectrum of such findings has been only sparsely described previously. The authors report cranial MRI findings in 12 patients with IE. Each of the patients had MRI evidence of cerebral embolization, with multiple brain lesions noted in most patients (n = 10). Cortical branch infarction was the most common lesion (n = 8), which usually involved the distal middle cerebral artery tree. The next most common finding (n = 7) was numerous small embolic lesions which typically lodged in the supratentorial gray-white junction, some of which were clinically silent and many of which enhanced (probable microabscesses). Brain hemorrhages were noted in four patients, most commonly subarachnoid hemorrhage (n = 3). Two patients developed multiple frank parenchymal macroabscesses/cerebritis lesions. A previously unreported finding in septic embolization, a stroke that became infected with abscess formation ("septic infarction"), was noted in two patients. MRI showed orbital cellulitis in two patients. Most patients studied with gadolinium showed enhancement of lesions (n = 5/8). The authors conclude that cranial MRI may be a valuable tool in the evaluation of patients with IE. The presence of characteristic cranial MRI lesions, especially of multiple types, may prompt early diagnosis and treatment.

The cerebral intravascular enhancement sign is not specific: a contrast-enhanced MRI study.

The intravascular enhancement (IVE) sign, also known as the "arterial enhancement sign", is an abnormal finding in the brain on contrast-enhanced MRI studies. IVE has been described in arterial cerebrovascular disorders, most commonly in acute or subacute arterial ischemic infarcts. However, the specificity of this sign has not been established. We describe four patients with disorders other than arterial strokes in whom gadolinium-enhanced high-field (1.5 T) MRI suggested IVE. The conditions were herpes simplex viral encephalitis, idiopathic cerebellitis, pneumococcal meningitis, and superior sagittal sinus thrombosis with venous infarction. IVE in these cases may be due to multiple factors, including arterial, venous, perivascular, and leptomeningeal or sulcal contrast medium accumulation. Our observations suggest that arterial ischemia, previously described as the cardinal cause of IVE, probably does not explain all instances, and urge caution in interpreting this sign as a specific MRI manifestation of acute arterial infarction or ischemia.

Cerebral venous infarctions presenting as enhancing space-occupying lesions: MRI findings.

Cerebral venous thrombosis is an unusual form of cerebrovascular disease that may cause cerebral venous infarction (CVI). Magnetic resonance imaging (MRI) of the brain may improve the often elusive diagnosis of CVI. However, the sensitivity, specificity, and full spectrum of such MRI findings are poorly understood. The authors present the cases of three patients with CVI whose MRI scans showed abnormally enhancing tumor-like brain lesions. Two of the CVIs were hemorrhagic and exerted mass effect. One patient showed increasingly nodular and heterogeneous ring-like enhancement progressing from the single-dose to the triple-dose gadolinium contrast images. The CVI of a second patient also showed ring-like enhancement. Biopsy was performed on one of these patients and was strongly considered for the other two patients to exclude neoplastic disease. Careful examination of the MRI appearance of venous structures and the use of specialized MRI techniques improved the recognition of CVI for two patients and prevented biopsy. This represents the first description of abnormal triple-dose MRI contrast enhancement in CVI. Consideration of CVI in the care of patients with enhancing tumor-like masses may lead to earlier diagnosis and treatment, preventing unnecessary invasive diagnostic procedures. CVI should be added to the differential diagnosis of supratentorial ring-enhancing masses.

High-resolution fluorodeoxyglucose positron emission tomography shows both global and regional cerebral hypometabolism in multiple sclerosis.

The authors study brain regional glucose metabolism prospectively in multiple sclerosis (MS) using high-resolution 2-[18-F]fluoro-2-deoxy-D-glucose positron emission tomography (FDG PET) in 25 MS patients of the Dent Neurologic Institute compared with 6 healthy subjects. Glucose metabolism is measured in 20 regions of interest using a line-profile technique. Compared with control subjects, a 9% reduction in total brain glucose metabolism is noted in MS patients (p < 0.05). Hypometabolism is widespread, including the cerebral cortex, subcortical nuclei, supratentorial white matter, and infratentorial structures. This reduction represents absolute regional decreases ranging from 3% to 18%. The most dramatic absolute reductions occur in the superior mesial frontal cortex, superior dorsolateral frontal cortex, mesial occipital cortex, lateral occipital cortex, deep inferior parietal white matter, and pons. The regional hypometabolism in the superior mesial frontal cortex and superior dorsolateral frontal cortex is statistically significant (p < 0.05), whereas the changes in the mesial occipital cortex (p = 0.07) and the lateral occipital cortex (p = 0.09) approach significance. The authors' findings suggest that widespread cerebral dysfunction occurs in MS, and that diaschisis or neuronal system disconnection resulting from white matter disease plays a major role. Cortical gray matter hypometabolism may also reflect direct MS involvement. The quantitative cerebral abnormalities detected by FDG PET may serve as a marker of disease activity in understanding the pathophysiological expression and therapeutic response of MS.

Neurosarcoidosis presenting as a large suprasellar mass. Magnetic resonance imaging findings.

We present unusual magnetic resonance imaging (MRI) findings in a case of neurosarcoidosis. MRI revealed a large solitary suprasellar mass which resembled a neoplasm. The lesion was isointense and hyperintense on T1-weighted images, hypointense on T2-weighted images, and intensely homogeneously enhancing. Biopsy revealed a polymorphous inflammatory lesion with giant cells, which extended from the hypothalamus, consistent with neurosarcoidosis. The diagnosis of neurosarcoidosis should be considered in patients presenting with large midline tumor-like suprasellar mass lesions.

Occipital lobe seizures as the major clinical manifestation of reversible posterior leukoencephalopathy syndrome: magnetic resonance imaging findings.

PURPOSE: Reversible posterior leukoencephalopathy syndrome (RPLS) is an increasingly recognized brain disorder most commonly associated with malignant hypertension, toxemia of pregnancy, or the use of immunosuppressive agents. When associated with acute hypertension, RPLS typically occurs concurrently with the fulminant clinical syndrome of hypertensive encephalopathy. We describe occipital lobe seizures, in the setting of only moderate elevations of blood pressure, as the major clinical manifestation of RPLS. METHODS: Two patients from the Dent Neurologic Institute are presented with clinical and magnetic resonance imaging (MRI) correlation. RESULTS: New onset secondarily generalized occipital seizures were noted, with MRI findings consistent with RPLS. Both of the patients had chronic renal failure and a moderate acute exacerbation of chronic hypertension. Other features of hypertensive encephalopathy were lacking, such as headache, nausea, papilledema, and an altered sensorium. Magnetic resonance imaging (MRI) showed edematous lesions primarily involving the posterior supratentorial white matter and corticomedullary junction, consistent with RPLS. With lowered blood pressure, the MRI lesions resolved and the patients became seizure-free without requiring chronic anticonvulsant therapy. CONCLUSIONS: Occipital seizures may represent the only major neurologic manifestation of RPLS due to acute hypertension, especially in patients with renal failure. Other evidence of hypertensive encephalopathy, such as cerebral signs and symptoms, need not be present. Blood pressure elevations may be only moderate. Early recognition of this readily treatable cause of occipital seizures may obviate the need for extensive, invasive investigations. Despite the impressive lesions on MRI, prompt treatment of this disorder carries a favorable prognosis.

Magnetic resonance imaging findings in acute cerebellitis.

Cerebellitis, also known as acute cerebellar ataxia, is an inflammatory syndrome of cerebellar dysfunction that may reflect an infectious, post-infectious, or post-vaccination disorder. We present serial magnetic resonance imaging (MRI) findings in a partially reversible, idiopathic cerebellitis. Bilateral cerebellar parenchymal abnormalities were noted, including hyperintensities on T2-weighted images and cerebellar swelling. After contrast administration, the cerebellum showed abnormal bilateral enhancement. The authors state this represents the first report of abnormal contrast enhancement in this condition. The MRI lesions most likely reflect the reversible, inflammatory nature of the syndrome.

Cognitive impairment after acute supratentorial stroke: a 6-month follow-up clinical and computed tomographic study.

To document the occurrence, time course, and predictors of global cognitive impairment following a supratentorial stroke, we prospectively studied 41 consecutive patients with acute cerebral ischemia and no evidence of pre-existing intellectual disturbances. The Graded Neurologic Scale and Mattis Dementia Rating Scale were used to assess neurologic and cognitive deficits within the first week, 3 weeks and 6 months after the onset of symptoms. CT was performed at each examination and semiquantitative measurements of infarct volumes and brain atrophy were obtained. Sixty-one percent of patients were found to be cognitively impaired within the first week. After 6 months this deficit had resolved in 24%, but was still present in 37% of individuals. Initial findings associated with a high risk of long-term intellectual dysfunction were: 1. moderately severe cognitive impairment, 2. diminished alertness in the acute stroke stage, 3. infarction involving the temporal lobe, 4. evidence of multiple brain infarcts and 5. pronounced ventricular enlargement. Logistic regression analysis revealed temporal infarcts and evidence of multiple ischemic lesions as the most powerful predictors of persistent cognitive impairment. By these two factors alone, 85.4% of study participants could be correctly classified regarding their cognitive outcome. These results suggest cognitive dysfunction to be a frequent sequela of supratentorial stroke. Its long-term persistence may be predicted on the basis of certain features.

Central nervous system lupus erythematosus: the value of magnetic resonance imaging.

Magnetic resonance imaging was sued to examine the brains of 13 patients with systemic lupus erythematosus (SLE) who had experienced symptoms and signs of encephalopathy. All the patients had normal computerized tomographic scans. Four patients with abnormal magnetic resonance imaging studies had active central nervous system disease. None of the 9 patients with normal scans had active nervous system involvement at the time of study. Parenchymal lesions were usually located in the region of the corticomedullary junction or in the deep periventricular white matter. In coronal sections, some of the corticomedullary lesions extended centripetally as thin irregular lines into the white matter approximating the course of penetrating arterioles of the brain. The parenchymal lesions resolved in 4 months in 1 patient, but persisted unchanged in the others despite clinical improvement or a stable clinical course. It is likely that the parenchymal lesions of these patients represent intrinsic vasculopathy of small cerebral vessels and perivascular microinfarctions associated with SLE.

Effect of nimodipine on blood pressure in acute ischemic stroke in humans.

Nimodipine is currently under investigation for the treatment of acute stroke. Although relatively specific for the cerebrovasculature, acute reductions in blood pressure after a dose may adversely affect neurologic outcome. We studied 29 consecutive acute ischemic stroke patients treated with placebo (n = 9) or either 120 (n = 10) or 240 (n = 10) mg/day of nimodipine. Blood pressure was recorded before and 30 and 60 minutes after a dose for the first 8 days. Ten neurologic physicians were asked to predict the treatment group (placebo or drug) of randomly selected patients based on blood pressure results. Only those patients on 240 mg/day of nimodipine had significant decreases in blood pressure after a dose (p less than 0.001); however, these were minimal (average 10 mm Hg systolic). Only 26 of 48 treatment predictions (54%) were correct. At the studied doses, nimodipine has a minimal effect on blood pressure in the acute stroke period.

Isolated idiopathic optic neuritis. Analysis of free kappa-light chains in cerebrospinal fluid and correlation with nuclear magnetic resonance findings.

There is controversy about the frequency with which patients with isolated optic neuritis (ON) subsequently develop clinically definite multiple sclerosis. Furthermore, at the time of isolated ON, there are no features that are both sensitive and accurate in predicting which patients will develop clinically definite multiple sclerosis. We analyzed cerebrospinal fluid (CSF) samples from eight patients with isolated ON and compared the result with the presence of clinically silent brain lesions demonstrated by nuclear magnetic resonance imaging. The single most common laboratory abnormality was an elevated level of free kappa-light chains in CSF. This abnormality was present in five (63%) of eight patients with isolated ON and correlated with the presence of clinically silent brain lesions demonstrated in four of the five patients by nuclear magnetic resonance. The only other laboratory abnormality that correlated with disseminated disease was the presence of oligoclonal bands, but this finding was observed less frequently than was an elevated level of free kappa-chains. Thus, the presence of free kappa-chains in CSF appears to correlate with disseminated disease in patients with isolated ON and may have prognostic value.