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Background and Purpose: White matter hyperintensities are a common magnetic resonance imaging (MRI) observation in the elderly. They are believed to represent a subclinical form of ischemic brain damage, but the underlying pathophysiological mechanisms are still incompletely understood. We postulated that oxidative mechanisms may favor the development of these changes and therefore correlated their presence and extent with the plasma concentrations of 10 naturally occurring antioxidants., Methods: We studied 355 clinically normal volunteers 45 to 75 years of age who were randomly selected from the official community register. A 1.5-T MRI of the brain and measurements of the plasma concentrations of antioxidants including zeaxanthin, cryptoxanthin, canthaxanthin, lycopene, alpha- and beta-carotene, retinol, gamma- and alpha-tocopherol, as well as ascorbate were performed in all study participants. White matter hyperintensities were graded as punctate, beginning confluent, and confluent abnormalities., Results: Punctate, beginning confluent, and confluent white matter abnormalities occurred in 101 (28.5%), 44 (12.4%), and 14 (3.9%) individuals, respectively. Study participants with white matter damage were significantly older and had a higher frequency of arterial hypertension and cardiac disease but lower serum concentrations of total cholesterol. The plasma levels of lycopene and alpha-tocopherol were significantly lower in subjects with early confluent and confluent white matter hyperintensities, while individuals with punctate foci had an antioxidant status similar to those with normal MRI scans. Alpha-tocopherol was the only antioxidant that remained significantly and inversely related to the presence of beginning confluent and confluent white matter changes after adjustment for the between-group differences in age, arterial hypertension, cardiac disease, and cholesterol. The adjusted odds ratio for early confluent and confluent white matter abnormalities was 3.70 (95% CI, 1.69 to 8.10) in the lowest compared with the highest quartile of the alpha-tocopherol concentration. The odds ratio increased to 7.11 (95% CI, 1.63 to 22.84) when quintiles of the alpha-tocopherol level were compared., Conclusions: These data do not prove a causal relation, but they provide evidence of an association between low plasma concentrations of vitamin E and a higher risk of cerebral white matter disease in elderly normal subjects.

We studied 20 patients aged 46-69 years (mean 57 years) undergoing long-term haemodialysis (HD) and 20 age- and sex-matched controls with single photon emission tomography (SPET) and 99Tcm-hexamethyl-propyleneamine-oxime to look for regional abnormalities in cerebral blood flow (CBF) and their relation to cognitive dysfunction. Global hemispheric tracer uptake relative to the cerebellum was similar in both groups, but regional over cerebellar activity was significantly reduced in the frontal cortex (85.9 +/- 5.1 vs 90.4 +/- 5.3; P = 0.01) and thalamus (99.2 +/- 8.8 vs 104.9 +/- 8.4; P = 0.05) of the HD patients. Normalization to whole-brain activity also showed the frontal cortex to be hypoactive in the HD patients, while tracer uptake was increased occipitally. These regional differences were not explained by the presence of atrophy or cerebrovascular damage seen on brain magnetic resonance imaging. The HD patients scored significantly worse on cognitive tests such as the Mini Mental State Examination (23 +/- 4 vs 28 +/- 1; P < 0.001) and Mattis Dementia Rating Scale (114 +/- 24 vs 143 +/- 1; P < 0.001). Regional activity ratios did not correlate with cognitive test scores, however. Our results indicate a disturbed pattern of CBF in HD patients, although regional SPET abnormalities did not correspond to the severity of cognitive dysfunction.

We reviewed a 7-year series of brain MRI examinations to determine the frequency and clinical significance of superficial siderosis of the central nervous system (SS). SS was defined by widespread bilateral signal loss at the surfaces of the cerebral or cerebellar hemispheres, the brain stem and the spinal cord on T2-weighted images. Clinical data comprised a neurological examination of identified patients and a review of their case notes. Among 8843 consecutive studies we identified 13 (0.15%) patients with MRI evidence of SS. Only 2 had symptoms or signs characteristic of SS, such as cerebellar ataxia, hearing loss, myelopathy and dementia. Haemosiderin deposition was most widespread in both symptomatic individuals. A definite cause for SS was detected in 9 patients (69%). None of them had a full clinical picture of SS. These data indicate SS per se to be much more frequent than may be assumed from the literature. It appears to become symptomatic only with extensive amounts of widespread iron deposition which develop preferentially with cryptic or unidentified causes of bleeding.

Purpose: To determine whether arteriolar vessel wall degeneration in primary intracerebral hematomas might be associated with ischemic brain lesions and clinically silent (apparently intracerebral) previous hemorrhages., Methods: The MR images of 120 consecutive patients (mean age, 60 years; age range, 22 to 84 years) with their first stroke caused by a primary intracerebral hematoma were reviewed retrospectively for coexisting ischemic damage and previous bleeds., Results: Early confluent to confluent white matter hyperintensities, lacunes, or infarction were present in 83 (69%) of the patients, and 39 (33%) had had previous hemorrhages consisting of microbleeds or old hematomas. Extensive white matter hyperintensities and lacunes were most frequent in patients with thalamic primary intracerebral hematomas. There was no relationship between the frequency of old hemorrhages and the location of subsequent primary intracerebral hematomas., Conclusion: Clinically silent ischemic lesions and previous hemorrhages are a common finding on MR images of patients with primary intracerebral hematoma. They may therefore serve as evidence of diffuse microangiopathy with a possible increased risk for cerebral hemorrhage.

We compared the magnetic resonance imaging results of 15 patients suffering from amyotrophic lateral sclerosis (ALS) with those of 30 age-matched controls to search for disease specific cerebral abnormalities. Symmetric hyperintensity along the corticospinal tract on the proton density spin-echo sequence was exclusively found in 4 ALS patients. It was associated with younger age, rapid disease progression and evolution of symptoms starting in the lower extremities. Signal loss of the motor cortex on T2-weighted images was frequently seen in ALS (9 patients) but was also observed in controls. As MRI is capable of providing direct evidence for ALS besides excluding other diseases it should be included in the diagnostic work-up of these patients.

The etiology of cerebral abnormalities after focal status epilepticus (SE) is unknown. Possible causes include hypoxia and the excessive release of excitatory amino acids. Magnetic resonance imaging (MRI) of a 21-year-old patient with "cryptogenic" continuous motor seizures showed swelling and signal hyperintensity of the contralateral parietotemporal cortex, the thalamus, and the ipsilateral cerebellum on T2-weighted images. These regions are connected by glutamatergic pathways. Proton magnetic resonance spectroscopy (MRS) of the cortical lesion yielded a signal peak at the resonance frequency of 2.29 ppm, suggesting a focal increase of glutamate or its degradation product glutamine. At 3-month follow-up, structural alterations had disappeared, but the N-acetyl-aspartate/choline ratio was still reduced in the previously abnormal area. These findings are the first to demonstrate the contribution of MRS to pathophysiologic studies of focal SE in humans and, in combination with the pattern of imaging abnormalities, support a major role of glutamate for seizure-related brain damage.

Background and Purpose: Our aim was to assess the association of elevated anticardiolipin antibody (aCL) titers with silent brain damage and cognitive functioning in middle-aged and elderly normal subjects., Methods: We determined the IgM and IgG aCL titers from 233 randomly selected clinically normal participants of a population-based stroke prevention study (age range, 44 to 82 years). aCL titers were categorized into negative (0 to 10 U/L), low positive (10 to 20 U/L), and moderately high positive (> 20 U/L). All participants underwent 1.5-T MRI and demanding neuropsychological testing. Semiautomated measurements of the total white matter hyperintensity area and the size of ventricles and cortical sulci were conducted., Results: There were 180 subjects (77.3%) with negative, 35 (15.0%) with low positive, and 18 (7.7%) with moderately high positive aCL titers. The frequency and extent of focal and diffuse brain abnormalities were not related to the aCL status of those examined. However, subjects with positive aCL results performed worse than those with negative findings on almost all tests administered, and this effect was mainly IgG titer related. When an ANCOVA test and partial correlations to correct for slight group differences in age and for the presence of major vascular risk factors were used, values of P < .05 were noted on tests assessing mnemonic and visuopractical abilities., Conclusion: Increased aCL titers in normal elderly persons may be associated with subtle neuropsychological dysfunction, but they do not appear to cause any morphological changes as demonstrated by MRI.