BMJ 1 Sep 2009 - Brain MRI

Incidental findings on brain magnetic resonance imaging
Aad van der Lugt
BMJ 2009;339 b3107

BMJ 17 Aug 2009

Study finds poor access to radiotherapy services in England
Roger Dobson
BMJ 2009;339 b3278

Incidental findings on brain magnetic resonance imaging: systematic review and meta-analysis
Zoe Morris, William N Whiteley, W T Longstreth, Jr, Frank Weber, Yi-Chung Lee, Yoshito Tsushima, Hannah Alphs, Susanne C Ladd, Charles Warlow, Joanna M Wardlaw, and Rustam Al-Shahi Salman
BMJ 2009;339 b3016

Articles from Neurology

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Tschampa, H J. ; Niehusmann, P ; Marek, M ; Mueller, C -A. ; Kuchelmeister, K ; Urbach, H
MRI in amyloid [beta]-related brain angiitis.
Neurology. 73(3):247, July 21, 2009.

Articles from Neurology

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MacDonald, C L. ; Schwarze, N ; Vaishnavi, S N. ; Epstein, A A. ; Snyder, A Z. et al
VERBAL MEMORY DEFICIT FOLLOWING TRAUMATIC BRAIN INJURY: ASSESSMENT USING ADVANCED MRI METHODS.
Neurology. 71(15):1199-1201, October 7, 2008.

Gronseth, G ; Cruccu, G ; Alksne, J ; Argoff, C ; Brainin, M ; Burchiel, K et al
Practice Parameter: The diagnostic evaluation and treatment of trigeminal neuralgia (an evidence-based review) : Report of the Quality Standards Subcommittee of the American Academy of Neurology and the European Federation of Neurological Societies.Neurology. 71(15):1183-1190, October 7, 2008. Abstract Background: Trigeminal neuralgia (TN) is a common cause of facial pain.Purpose: To answer the following questions: 1) In patients with TN, how often does routine neuroimaging (CT, MRI) identify a cause? 2) Which features identify patients at increased risk for symptomatic TN (STN; i.e., a structural cause such as a tumor)? 3) Does high-resolution MRI accurately identify patients with neurovascular compression? 4) Which drugs effectively treat classic and symptomatic trigeminal neuralgia? 5) When should surgery be offered? 6) Which surgical technique gives the longest pain-free period with the fewest complications and good quality of life?Methods: Systematic review of the literature by a panel of experts.Conclusions: In patients with trigeminal neuralgia (TN), routine head imaging identifies structural causes in up to 15% of patients and may be considered useful (Level C). Trigeminal sensory deficits, bilateral involvement of the trigeminal nerve, and abnormal trigeminal reflexes are associated with an increased risk of symptomatic TN (STN) and should be considered useful in distinguishing STN from classic trigeminal neuralgia (Level B). There is insufficient evidence to support or refute the usefulness of MRI to identify neurovascular compression of the trigeminal nerve (Level U). Carbamazepine (Level A) or oxcarbazepine (Level B) should be offered for pain control while baclofen and lamotrigine (Level C) may be considered useful. For patients with TN refractory to medical therapy, Gasserian ganglion percutaneous techniques, gamma knife, and microvascular decompression may be considered (Level C). The role of surgery vs pharmacotherapy in the management of TN in patients with MS remains uncertain.

Fischer, D ; Kley, R A. ; Strach, K ; Meyer, C ; Sommer, T ; Eger, K ; Rolfs, A et al
Distinct muscle imaging patterns in myofibrillar myopathies
Neurology. 71(10):758-765, September 2, 2008.
Abstract Objective: To compare muscle imaging findings in different subtypes of myofibrillar myopathies (MFM) in order to identify characteristic patterns of muscle alterations that may be helpful to separate these genetic heterogeneous muscular disorders.Methods: Muscle imaging and clinical findings of 46 patients with MFM were evaluated (19 desminopathy, 12 myotilinopathy, 11 filaminopathy, 1 [alpha]B-crystallinopathy, and 3 ZASPopathy). The data were collected retrospectively in 43 patients and prospectively in 3 patients.Results: In patients with desminopathy, the semitendinosus was at least equally affected as the biceps femoris, and the peroneal muscles were never less involved than the tibialis anterior (sensitivity of these imaging criteria to detect desminopathy in our cohort 100%, specificity 95%). In most of the patients with myotilinopathy, the adductor magnus showed more alterations than the gracilis muscle, and the sartorius was at least equally affected as the semitendinosus (sensitivity 90%, specificity 93%). In filaminopathy, the biceps femoris and semitendinosus were at least equally affected as the sartorius muscle, and the medial gastrocnemius was more affected than the lateral gastrocnemius. The semimembranosus mostly showed more alterations than the adductor magnus (sensitivity 88%, specificity 96%). Early adult onset and cardiac involvement was most often associated with desminopathy. In patients with filaminopathy, muscle weakness typically beginning in the 5th decade of life was mostly pronounced proximally, while late adult onset (>50 years) with distal weakness was more often present in myotilinopathy.Conclusions: Muscle imaging in combination with clinical data may be helpful for separation of distinct myofibrillar myopathy subtypes and in scheduling of genetic analysis.

Whitwell, J L. ; Josephs, K A. ; Murray, M E. ; Kantarci, K ; Przybelski, S A. ; Weigand, S D.
MRI correlates of neurofibrillary tangle pathology at autopsy: A voxel-based morphometry study
Neurology. 71(10):743-749, September 2, 2008. Abstract Background: Neurofibrillary tangles (NFTs), composed of hyperphosphorylated tau proteins, are one of the pathologic hallmarks of Alzheimer disease (AD). We aimed to determine whether patterns of gray matter atrophy from antemortem MRI correlate with Braak staging of NFT pathology.Methods: Eighty-three subjects with Braak stage III through VI, a pathologic diagnosis of low- to high-probability AD, and MRI within 4 years of death were identified. Voxel-based morphometry assessed gray matter atrophy in each Braak stage compared with 20 pathologic control subjects (Braak stages 0 through II).Results: In pairwise comparisons with Braak stages 0 through II, a graded response was observed across Braak stages V and VI, with more severe and widespread loss identified at Braak stage VI. No regions of loss were identified in Braak stage III or IV compared with Braak stages 0 through II. The lack of findings in Braak stages III and IV could be because Braak stage is based on the presence of any NFT pathology regardless of severity. Actual NFT burden may vary by Braak stage. Therefore, tau burden was assessed in subjects with Braak stages 0 through IV. Those with high tau burden showed greater gray matter loss in medial and lateral temporal lobes than those with low tau burden.Conclusions: Patterns of gray matter loss are associated with neurofibrillary tangle (NFT) pathology, specifically with NFT burden at Braak stages III and IV and with Braak stage itself at higher stages. This validates three-dimensional patterns of atrophy on MRI as an approximate in vivo surrogate indicator of the full brain topographic representation of the neurodegenerative aspect of Alzheimer disease pathology.

Articles from Neurology

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Virtanen, J K. ; Siscovick, D S.; Longstreth, W T. Jr ; Kuller, L H.
Fish consumption and risk of subclinical brain abnormalities on MRI in older adults
Neurology. 71(6):439-446, August 5, 2008.
Abstract
Objective: To investigate the association between fish consumption and subclinical brain abnormalities.Methods: In the population-based Cardiovascular Health Study, 3,660 participants age >=65 underwent an MRI scan in 1992-1994. Five years later, 2,313 were scanned. Neuroradiologists assessed MRI scans in a standardized and blinded manner. Food frequency questionnaires were used to assess dietary intakes. Participants with known cerebrovascular disease were excluded from the analyses.Results: After adjustment for multiple risk factors, the risk of having one or more prevalent subclinical infarcts was lower among those consuming tuna/other fish >=3 times/week, compared to <1/month ci =" 0.54-1.01," p =" 0.06," trend =" 0.03)."

Desikan, R S. ; Fischl, B ; Cabral, H J. ; Kemper, T L. ; Guttmann, C R. ; Blacker, D et al
MRI measures of temporoparietal regions show differential rates of atrophy during prodromal AD
Neurology. Status Publish Ahead of Print, POST AUTHOR CORRECTIONS, 30 July 2008 Background: MRI studies have demonstrated differential rates of atrophy in the entorhinal cortex and hippocampus during the prodromal phase of Alzheimer disease (AD). The current study was designed to determine whether a broader set of temporoparietal regions show differential rates of atrophy during the evolution of AD.Methods: Sixteen regions of interest (ROIs) were analyzed on MRI scans obtained at baseline and follow-up in 66 subjects comprising three groups: controls = individuals who were cognitively normal at both baseline and follow-up; nonconverters = subjects with mild cognitive impairment (MCI) at both baseline and follow-up; converters had MCI at baseline but had progressed to AD at follow-up.Results: Annualized percent change was analyzed with multivariate analysis of variance (MANOVA), covaried for age. The MANOVA demonstrated an effect of group (p = 0.004). Post hoc comparisons demonstrated greater rates of atrophy for converters vs nonconverters for six ROIs: hippocampus, entorhinal cortex, temporal pole, middle temporal gyrus, fusiform gyrus, and inferior temporal gyrus. Converters showed differentially greater rates of atrophy than controls in five of the same ROIs (and inferior parietal lobule). Rates of change in clinical status were correlated with the atrophy rates in these regions. Comparisons between controls and nonconverters demonstrated no differences.Conclusion: These results demonstrate that temporoparietal regions show differential rates of atrophy on MRI during prodromal Alzheimer disease (AD). MRI data correlate with measures of clinical severity and cognitive decline, suggesting the potential of these regions of interest as antemortem markers of prodromal AD.(C)2008AAN Enterprises, Inc.

BMC Medical Imaging 2008, 8:9 (23 May 2008

Research article Automatic volumetry on MR brain images can support diagnostic decision makingHeckemann RA, Hammers A, Rueckert D, Aviv RI, Harvey CJ, Hajnal JV
BMC Medical Imaging 2008, 8:9 (23 May 2008)[Abstract] [Provisional PDF] [PubMed]