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BRAINLIFE NEWSLETTER
Volume 5, Number 35 - 28 August 2006

Volume 5
Archive


1: AJNR Am J Neuroradiol. 2006 Jun-Jul;27(6):1362-9.
 
Apparent diffusion coefficients for differentiation of cerebellar tumors in children.

Rumboldt Z, Camacho DL, Lake D, Welsh CT, Castillo M.

Department of Radiology, Medical University of South Carolina, 169 Ashley Avenue, Charleston, SC 29425, USA.

BACKGROUND AND PURPOSE: Diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) maps provide information at MR imaging that may reflect cell attenuation and integrity. We hypothesized that cerebellar tumors in children can be differentiated by their ADC values. METHODS: Brain MR imaging studies that included ADC maps were retrospectively reviewed in 32 patients with histologically proved cerebellar neoplasm. There were 17 juvenile pilocytic astrocytomas (JPA), 8 medulloblastomas, 5 ependymomas, and 2 rhabdoid (atypical teratoid/rhabdoid tumor [AT/RT]) tumors. Absolute ADC values of contrast-enhancing solid tumor regions and ADC ratios (ADC of solid tumor to ADC of normal-appearing white matter) were compared with the histologic diagnosis. ADC values and ratios of JPAs, medulloblastomas, and ependymomas were compared by using a 2-tailed t test and one-way analysis of variance (ANOVA). RESULTS: ADC values were significantly higher in pilocytic astrocytomas (1.65 +/- 0.27) (mean +/- SD) than in ependymomas (1.10 +/- 0.11) (P = .0003) and medulloblastomas (0.66 +/- 0.15) (P < .0001). Ependymomas demonstrated significantly higher ADC values than medulloblastomas (P = .0005). The observed differences were statistically significant on ANOVA (P < .001). ADC ratios were also significantly different among these 3 tumor types. AT/RT ADC values were similar to medulloblastoma. The range of ADC values and ratios within JPAs and ependymomas did not overlap with that of medulloblastomas. CONCLUSION: Assessment of ADC values of enhancing solid tumor is a simple and reliable technique for preoperative differentiation of cerebellar tumors in pediatric patients. Our cutoff values of >1.4 x 10(3) mm(2)/s for JPA and <0.9 x 10(3) mm(2)/s for medulloblastoma were 100% specific.

PMID: 16775298 [PubMed - indexed for MEDLINE]

 
2: AJNR Am J Neuroradiol. 2006 Jun-Jul;27(6):1307-11.
 
Focal T2 hyperintensity in the dorsal brain stem in patients with vestibular schwannoma.

Okamoto K, Furusawa T, Ishikawa K, Sasai K, Tokiguchi S.

Center for Integrated Human Brain Science, Brain Research Institute, Niigata University, 1-757 Asahimachi-dori, Niigata 951-8585, Japan.

BACKGROUND AND PURPOSE: The vestibular nucleus cannot be visualized on MR imaging, but some patients with vestibular schwannoma show a tiny area of hyperintensity in the dorsal brain stem on T2-weighted images. The aim of this study was to determine whether this tiny area is characteristic of vestibular schwannoma. METHODS: We retrospectively reviewed the postoperative MR images of 53 patients with cerebellopontine angle tumor. MR images were obtained with a 1.5T scanner. Spin-echo pre- and postcontrast 3-mm-thick T1-weighted axial images, 3-mm-thick fast spin-echo (FSE) T2-weighted axial images, and 0.8-mm-thick constructive interference in steady state (CISS) axial images were acquired. Surgical and histopathologic diagnosis was vestibular schwannoma (41/53 = 77%), meningioma (7/53 = 13%), epidermoid cyst (3/53 = 6%), glioma with exophytic growth (1/53 = 2%), and chordoma (1/53 = 2%). RESULTS: A tiny area of hyperintensity was observed at the lateral angle of the fourth ventricle floor in 6 patients (3 men, 3 women; age range, 24-54 years; mean age, 43 years) with vestibular schwannoma larger than 2 cm in maximal diameter on both FSE T2-weighted and CISS images. Preoperative MR images with the same pulse sequences showed the same area of hyperintensity in all these patients. CONCLUSION: Because the location of the area of hyperintensity is coincident with the vestibular nucleus, the hyperintensity may represent degeneration of the nucleus. This hyperintensity should not be confused with a postoperative lesion or a small infarction. If such hyperintensity is seen in a patient with a large cerebellopontine angle tumor, a diagnosis of vestibular schwannoma is suggested.

PMID: 16775286 [PubMed - indexed for MEDLINE]

 
3: AJNR Am J Neuroradiol. 2006 Jun-Jul;27(6):1204-10.
 
Two patients with intraspinal germinoma associated with Klinefelter syndrome: case report and review of the literature.

Nakata Y, Yagishita A, Arai N.

Department of Neuroradiology, Tokyo Metropolitan Neurological Hospital, 2-6-1 Musashi-dai, Fuchu, Tokyo 183-0042, Japan.

We report 2 cases of intraspinal germinoma associated with Klinefelter syndrome. In one patient, spinal cord atrophy was observed at the upper and lower ends of the intraspinal tumor. Brain atrophy was observed in both cases. Germinoma should be included in the differential diagnosis if an intraspinal tumor is observed in a patient with Klinefelter syndrome.

Publication Types:
  • Case Reports

PMID: 16775265 [PubMed - indexed for MEDLINE]

 
4: Eur J Cancer. 2006 Jun;42(9):1298-308. Epub 2006 May 12.
 
Neural stem cells as novel cancer therapeutic vehicles.

Yip S, Sabetrasekh R, Sidman RL, Snyder EY.

Department of Pathology & Laboratory Medicine, Vancouver General Hospital, University of British Columbia, Vancouver, BC, Canada.

The startling resemblance of many of the behaviours of brain tumours to the intrinsic properties of the neural stem/progenitor cell has triggered a recent dual interest in arming stem cells to track and help eradicate tumours and in viewing stem cell biology as somehow integral to the emergence and/or propagation of the neoplasm itself. These aspects are reviewed and discussed here.

Publication Types:
  • Review

PMID: 16697638 [PubMed - indexed for MEDLINE]4

 
5: Eur J Cancer. 2006 Jun;42(9):1237-42. Epub 2006 May 2.
 
Brain cancer stem-like cells.

Kondo T.

Centre for Brain Repair, University of Cambridge, Cambridge CB2 2PY, UK. tkondo@cdb.riken.jp

Both stem cells and cancer cells are thought to be capable of unlimited proliferation. Moreover, many tumours and cancer cell lines express stem cell markers, including adenosine triphosphate (ATP)-binding cassette transporters, by which the cells pump out specific fluorescent dyes as well as anti-cancer drugs, suggesting either that cancer cells resemble stem cells or that cancers contain stem-like cells. Using the common characteristics of brain tumour cells and neural stem cells, several research groups have succeeded in identifying stem-like cells (cancer stem-like cells) in brain tumours and brain cancer cell lines. The purified cancer stem-like cells, but not the other cancer cells, self-renew and form tumours when transplanted in vivo. Thus, cancer stem-like cells in brain tumours might be a crucial target for anti-brain tumour therapy.

Publication Types:
  • Review

PMID: 16632342 [PubMed - indexed for MEDLINE]4

 
6: Int J Cancer. 2006 Sep 1;119(5):1136-44.
 
Brain cancer mortality and potential occupational exposure to lead: findings from the National Longitudinal Mortality Study, 1979-1989.

van Wijngaarden E, Dosemeci M.

Division of Epidemiology, Department of Community and Preventive Medicine, University of Rochester School of Medicine and Dentistry, NY 14642, USA. edwin_van_wijngaarden@urmc.rochester.edu

We evaluated the association between potential occupational lead exposure and the risk of brain cancer mortality in the National Longitudinal Mortality Study (NLMS), which is a prospective census-based cohort study of mortality among the noninstitutionalized United States population (1979-1989). The present study was limited to individuals for whom occupation and industry were available (n = 317,968). Estimates of probability and intensity of lead exposure were assigned using a job-exposure matrix (JEM). Risk estimates for the impact of lead on brain cancer mortality were computed using standardized mortality ratio (SMR) and proportional hazards and Poisson regression techniques, adjusting for the effects of age, gender and several other covariates. Brain cancer mortality rates were greater among individuals in jobs potentially involving lead exposure as compared to those unexposed (age- and gender-adjusted hazard ratio (HR) = 1.5; 95% confidence interval (CI) = 0.9-2.3) with indications of an exposure-response trend (probability: low HR = 0.7 (95% CI = 0.2-2.2), medium HR = 1.4 (95% CI = 0.8-2.5), high HR = 2.2 (95% CI = 1.2-4.0); intensity: low HR = 1.2 (95% CI = 0.7-2.1), medium/high HR = 1.9 (95% CI = 1.0-3.4)). Brain cancer risk was greatest among individuals with the highest levels of probability and intensity (HR = 2.3; 95% CI = 1.3-4.2). These findings provide further support for an association between occupational lead exposure and brain cancer mortality, but need to be interpreted cautiously due to the consideration of brain cancer as one disease entity and the absence of biological measures of lead exposure. Copyright 2006 Wiley-Liss, Inc.

PMID: 16570286 [PubMed - indexed for MEDLINE]4

 
7: J Clin Oncol. 2006 Aug 20;24(24):4037; author reply 4037-8.
 
Influence of whole-brain radiotherapy on remission of brain metastases.

Nieder C.

Publication Types:
  • Comment
  • Letter

PMID: 16921062 [PubMed - in process]3

 
8: J Clin Oncol. 2006 Aug 20;24(24):3871-9.
 
Phase III trial of carmustine and cisplatin compared with carmustine alone and standard radiation therapy or accelerated radiation therapy in patients with glioblastoma multiforme: North Central Cancer Treatment Group 93-72-52 and Southwest Oncology Group 9503 Trials.

Buckner JC, Ballman KV, Michalak JC, Burton GV, Cascino TL, Schomberg PJ, Hawkins RB, Scheithauer BW, Sandler HM, Marks RS, O'Fallon JR; North Central Cancer Treatment Group 93-72-52; Southwest Oncology Group 9503 Trials.

Mayo Clinic and Mayo Foundation, Rochester, MN 55905, USA. buckner.jan@mayo.edu

PURPOSE: In patients with newly diagnosed glioblastoma multiforme, to determine whether cisplatin plus carmustine (BCNU) administered before and concurrently with radiation therapy (RT) improves survival compared with BCNU and RT and whether survival using accelerated RT (ART) is equivalent to survival using standard RT (SRT). PATIENTS AND METHODS: After surgery, patients were stratified by age, performance score, extent of surgical resection, and histology (glioblastoma v gliosarcoma) and then randomly assigned to arm A (BCNU plus SRT), arm B (BCNU plus ART), arm C (cisplatin plus BCNU plus SRT), or arm D (cisplatin plus BCNU plus ART). RESULTS: Four hundred fifty-one patients were randomly assigned, and 401 were eligible. Frequent toxicities included myelosuppression, vomiting, sensory neuropathy, and ototoxicity and were worse with cisplatin. There was no difference in toxicity between SRT and ART. Median survival times and 2-year survival rates for patients who received BCNU plus RT (arms A and B) compared with cisplatin, BCNU, and RT (arms C and D) were 10.1 v 11.5 months, respectively, and 11.5% v 13.7%, respectively (P = .19). Median survival times and 2-year survival rates for patients who received SRT (arms A and C) compared with ART (arms B and D) were 11.2 v 10.5 months, respectively, and 13.8% v 11.4%, respectively (P = .33). CONCLUSION: Cisplatin administered concurrently with BCNU and RT resulted in more toxicity but provided no significant improvement in survival. SRT and ART produced similar toxicity and survival.

PMID: 16921039 [PubMed - in process]3

 
9: J Neurochem. 2006 Sep;98(5):1497-506.
 
RNA interference targeting protein tyrosine phosphatase zeta/receptor-type protein tyrosine phosphatase beta suppresses glioblastoma growth in vitro and in vivo.

Ulbricht U, Eckerich C, Fillbrandt R, Westphal M, Lamszus K.

Department of Neurosurgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

The protein tyrosine phosphatase zeta/receptor-type protein tyrosine phosphatase beta (PTPzeta/RPTPbeta) and its ligand pleiotrophin (PTN) are overexpressed in human glioblastomas. Both molecules are involved in neuronal cell migration during CNS development. In addition, PTN can induce glioma cell migration which is at least in part mediated through binding to PTPzeta/RPTPbeta. To study the relevance of this ligand-receptor pair for glioma growth in vitro and in vivo, we transfected the human glioblastoma cell line U251-MG with small interfering RNA (siRNA) directed against PTPzeta/RPTPbeta. Stable siRNA transfection resulted in strong down-regulation of PTPzeta/RPTPbeta expression. When injected subcutaneously into nude mice, clones that expressed normal levels of PTPzeta/RPTPbeta (PTPzeta + clones) formed exponentially growing tumours, whereas tumour growth was almost completely abrogated for clones that expressed reduced PTPzeta/RPTPbeta levels (PTPzeta - clones). Similar results were obtained using an orthotopic intracerebral model. Proliferation of PTPzeta - cells in vitro was significantly reduced compared with that of control clones. Matrix-immobilized PTN stimulated the proliferation of PTPzeta + cells but not of PTPzeta - cells. Haptotactic migration induced by PTN was reduced for PTPzeta - clones compared with control clones. Our findings suggest that antagonization of PTPzeta/RPTPbeta expression can inhibit glioma growth in vivo and may thus represent a potentially promising treatment strategy.

PMID: 16923162 [PubMed - in process]

 
10: J Neurol Neurosurg Psychiatry. 2006 Sep;77(9):1099-100.
 
Misoplegia: a review of the literature and a case without hemiplegia.

Loetscher T, Regard M, Brugger P.

Publication Types:
  • Case Reports
  • Letter

PMID: 16914766 [PubMed - indexed for MEDLINE]

 
11: J Neurol Neurosurg Psychiatry. 2006 Sep;77(9):1097.
 
Neurogenic pulmonary oedema in a patient with leptomeningeal carcinomatosis.

Dammers R, van den Bent MJ.

Publication Types:
  • Case Reports
  • Letter

PMID: 16914765 [PubMed - indexed for MEDLINE]

 
12: J Neurol Neurosurg Psychiatry. 2006 Sep;77(9):1078.
 
Neurological picture. Torcular Erdheim-Chester disease.

Gazzeri R, Galarza M, Amoroso R, De Bonis C, D'Angelo V.

Department of Neurosurgery, San Giovanni Addolorata Hospital, Rome, Italy. robertogazzeri@gmail.com

Publication Types:
  • Case Reports

PMID: 16914757 [PubMed - indexed for MEDLINE]

 
13: J Neurooncol. 2006 May;78(1):41-6. Epub 2006 Mar 31.
 
Predicting which children are at risk for ependymoma relapse.

Sowar K, Straessle J, Donson AM, Handler M, Foreman NK.

University of Colorado at Denver and Health Sciences Center (UCDHSC) and Denver Children's Hospital, Denver, Colorado 80045, USA.

Ependymomas account for 6-12% of all pediatric intracranial tumors. Despite complete resection and radiation, about 50% of patients relapse and have subsequent dismal prognoses. As no clinical findings reliably forecast tumor recurrence, we sought to determine if gene expression profiling could be used to distinguish patients at high risk for relapse at initial diagnosis, and thereby make them candidates for innovative treatments at an early stage. We extracted RNA from 13 ependymoma specimens: 7 from patients who experienced tumor recurrence, and 6 from patients who have not recurred. RNA was applied to Affymetrix HG-U133 plus 2.0 microarray chips, and microarrays were analyzed with GeneSpring 7.0 and Prediction Analysis of Microarrays (PAM) software. The 3-gene subset of PLEK (pleckstrin), NF-kappaB2 (nuclear factor kappa beta-2), and LOC374491 (TPTE and PTEN homologous inositol phosphatase pseudogene) was identified as the minimal subset capable of accurately distinguishing tumors according to recurrence. In summary, gene expression profiling may be valuable, perhaps in combination with clinical findings identified in some studies, for identifying children at high risk for ependymoma relapse.

PMID: 16575538 [PubMed - indexed for MEDLINE]3

 
14: J Neurooncol. 2006 May;78(1):59-62.
 
Development of contrast enhancement after long-term observation of a dysembryoplastic neuroepithelial tumor.

Jensen RL, Caamano E, Jensen EM, Couldwell WT.

Department of Neurosurgery, University of Utah, Salt Lake City, Utah 84132-2303, USA. randy.jensen@hsc.utah.edu

Dysembryoplastic neuroepithelial tumors (DNET) are usually benign lesions that arise in cortical regions and are discovered after new onset of seizure. These lesions have many different imaging characteristics. We report a patient with a presumed low-grade medial temporal lobe lesion that was followed for many years without any change in size or imaging characteristics. This previously non-enhancing tumor evolved to become contrast enhanced on routine imaging without apparent tumor growth. The patient underwent surgery, and the pathology was confirmed as a DNET with no atypical changes. This case demonstrates the potential that DNETs may exhibit a changing MRI pattern over time. Natural history, imaging characteristics, and management are reviewed.

PMID: 16314940 [PubMed - indexed for MEDLINE]

 
15: J Neurooncol. 2006 May;78(1):63-9. Epub 2005 Nov 29.
 
Hypofractionated radiotherapy boost for dose escalation as a treatment option for high-grade spinal cord astrocytic tumor.

Katoh N, Shirato H, Aoyama H, Onimaru R, Suzuki K, Hida K, Miyasaka K, Iwasaki Y.

Department of Radiology, Hokkaido University School of Medicine, Sapporo, Japan. noriwo@radi.med.hokudai.ac.jp

PURPOSE: To retrospectively analyze the outcome of post-operative radiotherapy for spinal cord glioma with the emphasis on the hypofractionated radiotherapy boost for dose escalation as a treatment option for high-grade spinal cord astrocytic tumors. MATERIALS AND METHODS: Forty-one patients with spinal cord glioma received post-operative radiotherapy between 1979 and 2003. The median age was 34 years (range, 10-66 years). Median follow-up was 49 months (range, 5-291 months). There were 12 low-grade astrocytic tumors, 11 high-grade astrocytic tumors, 16 low-grade ependymal tumors and 2 high-grade ependymal tumors. Among 11 patients with high-grade astrocytic tumors, 5 with anaplastic astrocytoma and 1 with glioblastoma received hypofractionated radiotherapy boost for dose escalation. The median total dose of the conventional radiotherapy was 45.5 Gy in 19 fractions (range, 30.0-60.0 Gy). The median normalized total dose (using daily dose of 2.0 Gy and an alpha/ per thousandbeta ratio of 2.0) of the hypofractionated radiotherapy boost was 131 Gy2 (range, 85-249). RESULTS: The Kaplan-Meier survival rates at 10 years from the date of the first surgery were 64% for the entire group, 47% for the astrocytic tumors and 84% for the ependymal tumors, respectively (P=0.009). Among 11 patients with high-grade astrocytic tumors, the actuarial survival rate at 10 years was 35%. The actuarial survival rates at 10 years were 67% for those who received hypofractionated radiotherapy boost for dose escalation, and 20% for those who did not (P=0.47). DISCUSSION: The results for ependymal tumors and low-grade astrocytic tumors were comparable to those reported in the literature. Hypofractionated radiotherapy boost for dose escalation may help to prolong the survival of patients with high-grade astrocytic tumors.

PMID: 16314938 [PubMed - indexed for MEDLINE]3

 
16: J Neurosurg. 2006 Aug;105(2):159-60; author reply 160.

Craniopharyngioma.

Fraioli MF, Contratti F.

Publication Types:
  • Comment
  • Letter

PMID: 16922083 [PubMed - in process]

 
17: J Neurosurg. 2006 Aug;105(2):134-9.

Intracranial aneurysm following radiation therapy during childhood for a brain tumor. Case report and review of the literature.

Sciubba DM, Gallia GL, Recinos P, Garonzik IM, Clatterbuck RE.

Department of Neurosurgery, The Johns Hopkins School of Medicine, Baltimore, Maryland 21287, USA.

Ionizing radiation therapy is associated with pathological vascular changes in intracranial vessels, most commonly in the form of vessel thrombosis and occlusion. The development of an intracranial aneurysm following such therapy, however, is far less common. In this report the authors describe a 24-year-old man in whom a distal middle cerebral artery aneurysm developed 15 years after radiotherapy, which was given as adjuvant treatment following resection of a medulloblastoma. The patient underwent a craniotomy for microsurgical trapping of the aneurysm and was discharged without any neurological deficit. This case serves to remind clinicians of the possibility, albeit rare, that intracranial aneurysms may form following cranial radiotherapy.

PMID: 16922075 [PubMed - in process]3

 
18: J Neurosurg. 2006 May;104(5 Suppl):362-5.

Basicranial diplomyelia: an extension of the split cord malformation theory. Case report.

Rustamzadeh E, Graupman PC, Lam CH.

Department of Neurosurgery, University of Minnesota, Minneapolis, Minnesota 55455, USA.

Basicranial diastematomyelia is an extremely rare congenital disorder. A review of the literature indicates only one reported case of basicranial diastematomyelia in which an osseous peg divided the brainstem in two. The authors present the first reported case of basicranial diplomyelia split by a fibrous band and correlate its pathogenesis with that of split cord malformation (SCM). The patient described in the present report had a fibrous stalk dividing the brainstem, and therefore the condition was categorized as a diplomyelia, or SCM Type II. Because the occipital dermatomes behave similarly to the spinal dermatomes early in development, they may be subject to the same embryonic error that results in SCM. The authors propose that the mechanism leading to SCM is the same as that found in basicranial split malformations and that the theory explaining it be modified to include the posterior fossa.

Publication Types:
  • Case Reports

PMID: 16848097 [PubMed - indexed for MEDLINE]

 
19: J Neurosurg. 2006 May;104(5 Suppl):348-51.

Navigated laser-assisted endoscopic fenestration of a suprasellar arachnoid cyst in a 2-year-old child with bobble-head doll syndrome. Case report.

Van Beijnum J, Hanlo PW, Han KS, Ludo Van der Pol W, Verdaasdonk RM, Van Nieuwenhuizen O.

Department of Neurosurgery, University Medical Center, Utrecht, The Netherlands. J.vanBeijnum@umcutrecht.nl

The authors present the case of a 2-year-old boy with bobble-head doll syndrome (BHDS) associated with a large suprasellar arachnoid cyst and enlarged ventricles, who was successfully treated with neuronavigated laser-assisted endoscopic ventriculocystocisternostomy. The clinical history, surgical treatment, and clinical follow up of the patient are described. A navigated laser-assisted endoscopic ventriculocystocisternostomy of the suprasellar arachnoid cyst led to cessation of the head bobbing, and notable reduction of the cyst and ventricles was visible on the postoperative magnetic resonance images. Caused by a suprasellar arachnoid cyst, BHDS can be successfully treated with navigated laser-assisted endoscopic ventriculocystocisternostomy. The advantages of this procedure are minimal invasiveness and facilitated guidance of the neuronavigation system to the target area when normal anatomical landmarks are not visible.

Publication Types:
  • Case Reports

PMID: 16848093 [PubMed - indexed for MEDLINE]

 
20: Radiology. 2006 Sep;240(3):803-10.
 
Gliomas: histopathologic evaluation of changes in directionality and magnitude of water diffusion at diffusion-tensor MR imaging.

Stadlbauer A, Ganslandt O, Buslei R, Hammen T, Gruber S, Moser E, Buchfelder M, Salomonowitz E, Nimsky C.

Department of Neurosurgery, Neurocenter, Departments of Neuropathology and Neurology, University of Erlangen-Nuremberg, Erlangen, Germany.

PURPOSE: To retrospectively correlate changes in fractional anisotropy (FA) and mean diffusivity in gliomas at diffusion-tensor magnetic resonance (MR) imaging with the degree of tumor cell infiltration determined histologically. MATERIALS AND METHODS: The institutional review board required neither ethics committee approval nor patient informed consent for this study. Twenty patients (eight women, 12 men; age range, 18-53 years) with glioma (seven World Health Organization grade II and 13 grade III tumors) underwent diffusion-tensor MR imaging at 1.5 T. Diffusion-tensor data were obtained with an echo-planar imaging sequence with six diffusion directions (b = 1000 sec/mm(2)), isotropic 1.9-mm voxels, and five averages. FA and mean diffusivity values were calculated from diffusion-tensor data. Coregistration with a three-dimensional MR imaging data set (used for stereotactic brain biopsies) enabled correlation of FA and mean diffusivity values with the histopathologic findings total cell number (CN), tumor CN, and percentage tumor infiltration (TI) by using linear, exponential, and logarithmic models. Student t and Mann-Whitney U tests were performed. RESULTS: Histopathologic findings of 77 MR image-guided stereotactic biopsies in all 20 patients were correlated with FA and mean diffusivity values at the biopsy locus. For FA and mean diffusivity, a logarithmic model showed strongest correlation with tumor CN and total CN; a linear model showed strongest correlation with percentage TI. For FA there were negative logarithmic (R = -0.802, P < .001) and linear (R = -0.796, P < .001) correlations with tumor CN and percentage TI, respectively. For mean diffusivity there were positive logarithmic (R = 0.557, P < .001) and linear correlations (R = 0.521, P < .001) with tumor CN and percentage TI, respectively. Differences between correlations for FA and mean diffusivity versus tumor CN (P < .001) and percentage TI (P < .001) were significant. CONCLUSION: FA is better than mean diffusivity for assessment and delineation of different degrees of pathologic changes (ie, TI) in glioma. (c) RSNA, 2006.

PMID: 16926329 [PubMed - in process]
 
 

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