Proton magnetic resonance spectroscopy (1H-MRS) offers a unique insight into brain cellular metabolism following traumatic brain injury (TBI). The aim of the present study was to assess change in neurometabolite markers of brain injury during the recovery period following TBI. We studied 19 TBI patients at 1.5, 3, and 6 months postinjury and 28 controls. We used 1H-MRS to quantify N-acetylaspartate (NAA), creatine (Cre), choline (Cho), and myoinositol (mIns) in occipitoparietal gray matter (GM) and white matter (WM) remote from the primary injury focus. Neuropsychological testing quantified cognitive impairment and recovery. At 1.5 months, we found cognitive impairment (mean z score = -1.36 vs. 0.18,p < 0.01), lower NAA (GM: 12.42 mM vs. 13.03, p = 0.01; WM: 11.75 vs. 12.81, p < 0.01), and elevated Cho (GM: 1.51 vs. 1.25, p < 0.01; WM: 1.98 vs. 1.79, p < 0.01) in TBI patients compared with controls. GM NAA at 1.5 months predicted cognitive function at outcome (6 months postinjury; r = 0.63, p = 0.04). GM NAA continued to fall by 0.46 mM between 1.5 and 3 months (p = 0.02) indicating continuing neuronal loss, metabolic dysfunction, or both. Between 3 and 6 months, WM NAA increased by 0.55 mM (p = 0.06) suggesting metabolic recovery. Patients with poorer outcomes had elevated mean GM Cho at 3 months postinjury, suggesting active inflammation, as compared to patients with better outcomes (p = 0.002). 1H-MRS offers a noninvasive approach to assessing neuronal injury and inflammation following TBI, and may provide unique data for patient management and assessment of therapeutic efficacy.

Objective Magnetic resonance imaging (MRI) often demonstrates brain lesions in neuropsychiatric systemic lupus erythematosus (NPSL). The present study compared post-mortem histopathology with pre-mortem MRI in NPSL. Methods 200 subjects with NPSLE were studied prospectively with MRI over a 10-year period during which 22 subjects died. In 14 subjects, a brain autopsy with histopathology that permitted direct comparison with pre mortem MRI was successfully obtained. Surface anatomy was used to determine the approximate location of individual lesions. Results Pre mortem MRI findings in fatal NPSLE were small focal white matter lesions (100%), cortical atrophy (64%), ventricular dilation (57%), cerebral edema (50%), diffuse white matter abnormalities (43%), focal atrophy (36%), cerebral infarction (29%), acute leukoencephalopathy (25%), intracranial hemorrhage (21%), and calcifications (7%). Microscopic findings in fatal NPSLE included global ischemic changes (57%), parenchymal edema (50%), microhemorrhages (43%), glial hyperplasia (43%), diffuse neuronal/axonal loss (36%), resolved cerebral infarction (33%), microthomboemboli (29%), blood vessel remodeling (29%), acute cerebral infarction (14%), acute macrohemorrhages (14%), and resolved intracranial hemorrhages (7%). Cortical atrophy and ventricular dilation seen by MRI predicted brain mass at autopsy (r = -0.72, p = 0.01, and r = -0.77, p =0.01, respectively). Cerebral autopsy findings, including infarction, cerebral edema, intracranial hemorrhage, calcifications, cysts, and focal atrophy were also predicted accurately by pre mortem MRI. Conclusion Brain lesions in NPSLE detected by MRI accurately represent serious underlying cerebrovascular and parenchymal brain injury on pathology.

No abstract

No abstract

Proton magnetic resonance spectroscopy (1H-MRS) offers a unique non-invasive approach to measurement of N-acetylaspartate (NAA) and choline (Cho), putative markers of neuronal and glial integrity. Previous studies revealed that these neurochemicals predict cognitive impairment in diseased subjects, although little is known about their relationship to cognitive functioning in healthy people. We measured the concentrations of NAA and Cho in the left occipitoparietal white matter of 26 healthy adults and compared them with intellectual performance assessed by the Wechsler Adult Intelligence Scale-3. We found that NAA (b = 0.6, p < 0.01) and Cho (b = -0.42, p < 0.01) were independently associated with the Full-Scale Intelligence Quotient. Together, these metabolites accounted for a large proportion of the variance in intelligence (r2 = 0.45). Possible mechanisms underlying these correlations, such as mitochondrial function and myelin turnover, are discussed. 1H-MRS is a sensitive new tool to assess the neuronal underpinnings of cognitive function non-invasively.

Objective To determine whether Libman-Sacks endocarditis is a pathogenic factor for cerebrovascular disease (CVD) in systemic lupus erythematosus (SLE). Background A cardioembolic pathogenesis of SLE CVD manifested as 1) neuropsychiatric SLE (NPSLE) including stroke and transient ischemic attacks (TIA), 2) neurocognitive dysfunction, and 3) MRI focal brain lesions has not been established. Methods A 6-year study of 30 patients with acute NPSLE (27 women, age 38±12 years), 46 age-and-sex matched SLE controls without NPSLE (42 women, age 36±12 years), and 26 age-and-sex matched healthy controls (22 women, age 34±11 years) who underwent clinical and laboratory evaluations, TEE, carotid duplex, transcranial Doppler, neurocognitive testing, and brain MRI/MRA. NPSLE patients were re-evaluated after 4.5 months of therapy. All patients were followed clinically for a median of 52 months. Results Libman-Sacks vegetations (87%), cerebromicroembolism (27% with 2.5 times more events per hour), neurocognitive dysfunction (60%), and cerebral infarcts (47%) were more common in NPSLE than in SLE (28%, 20%, 33%, and 0%) and healthy controls (8%, 0%, 4%, and 0%, respectively) (all p≤0.009). Patients with vegetations had 3 times more cerebromicroemboli per hour, lower cerebral blood flow, more stroke/TIA and overall NPSLE events, neurocognitive dysfunction, cerebral infarcts, and brain lesion load than those without (all p≤0.01). Libman-Sacks vegetations were independent risk factors of NPSLE (OR=13.4, p<0.001), neurocognitive dysfunction (OR=8.0, p=0.01), brain lesions (OR=5.6, p=0.004), and all 3 outcomes combined (OR=7.5, p<0.001). Follow-up re-evaluations in 18 (78%) of 23 surviving NPSLE patients demonstrated improvement of vegetations, microembolism, brain perfusion, neurocognitive dysfunction, and lesion load (all p≤0.04). Finally, patients with vegetations had reduced event free survival time to stroke/TIA, cognitive disability, or death (p=0.007). Conclusion The presence of Libman-Sacks endocarditis in patients with SLE is associated with higher risk for embolic CVD. This suggests that Libman-Sacks endocarditis may be a source of cerebral emboli.

US-guided arthrocentesis and injection of the knee are superior to anatomic landmark palpation-guided arthrocentesis, resulting in significantly less procedural pain, improved arthrocentesis success, greater synovial fluid yield, more complete joint decompression, and improved clinical outcomes.

BackgroundNeuropsychiatric systemic lupus erythematosus (NPSLE) is associated with increased morbidity and mortality.MethodsWe used Diffusion Tensor Imaging (DTI) to assess white matter abnormalities in seventeen NPSLE patients, sixteen SLE patients without NPSLE, and twenty age- and gender-matched controls.ResultsNPSLE patients differed significantly from SLE and control patients in white matter integrity of the body of the corpus callosum, the left arm of the forceps major and the left anterior corona radiata.ConclusionsSeveral possible mechanisms of white matter injury are explored, including vascular injury, medication effects, and platelet or fibrin macro- or microembolism from Libman-Sacks endocarditis.