Intraoperative clinical testing overestimates the therapeutic window of the permanent DBS electrode in the subthalamic nucleus.

BACKGROUND: Intraoperative test stimulation is established to optimize target localization in STN DBS, but requires a time-consuming awake surgery in off-medication state. The aim of this study was to compare the thresholds of stimulation-induced effects of test stimulation and the permanent electrode. METHODS: Fifty-nine PD patients receiving bilateral STN DBS were clinically examined with stepwise increasing monopolar stimulation during surgery and DBS programming at matched stimulation depths. Thresholds of therapeutic and side effects were obtained from standardized examination protocols. RESULTS: Postoperative stimulation via the permanent electrode caused side effects at a significantly lower threshold than predicted during intraoperative test stimulation (P < 0.001); whereas sufficient therapeutic effects were achieved at significantly higher thresholds (P < 0.001). CONCLUSIONS: Intraoperative testing may lead to an overestimation of the therapeutic window. The two different electrodes lead to distinct spreading of the electric field in the STN and surrounding tissues that causes different volume of tissue activated (VTA). Clinicians involved in DBS surgery and programming should be aware of the differences in both stimulation settings, concerning electrodes geometry, stimulation modes as well as the impact of time. Therapeutic and side effects of permanent stimulation are not predictable by intraoperative test stimulation. Test stimulation may be an orientating test for very low thresholds of side effects instead.

Ocular color-coded sonography - a promising tool for neurologists and intensive care physicians.

Ocular color-coded duplex sonography (OCCS), when performed within the safety limits of diagnostic ultrasonography, is an easy noninvasive technique with high potential for diagnosis and therapy in diseases with raised intracranial pressure and vascular diseases affecting the eye. Despite the capabilities of modern ultrasound systems and its scientific validation, OCCS has not gained widespread use in neurological practice. In this review, the authors describe the technique and main parameter settings of OCCS systems to reduce potential risks as thermal or cavitational effects for sensitive orbital structures. Applications of OCCS are the determination of intracranial pressure in emergency medicine, and follow-up evaluations of idiopathic intracranial hypertension and ventricular shunting by measuring the optic nerve sheath diameter. A diameter of 5.7 - 6.0 mm corresponds well with symptomatically increased intracranial pressure (> 20 cmH2O). OCCS also helps to discriminate between different etiologies of central retinal artery occlusion - by visualization of a "spot sign" and Doppler flow analysis of the central retinal artery - and aids the differential diagnosis of papilledema. At the end perspectives are illustrated that combine established ultrasound methods such as transcranial color-coded sonography with OCCS.

The retrobulbar "spot sign" as a discriminator between vasculitic and thrombo-embolic affections of the retinal blood supply.

PURPOSE: Sudden retinal blindness is a common complication of temporal arteritis (TA). Another common cause is embolic occlusion of the central retinal artery (CRA). The aim of this prospective study was to examine the diagnostic value of hyperechoic material in the CRA for the exclusion of vasculitis as a cause. The authors used orbital color-coded sonography (OCCS) for the detection of hyperechoic material. MATERIALS AND METHODS: 24 patients with sudden vision loss were included in the study after the exclusion of other causes (e. g. vitreous bleeding, retinal detachment). Parallel to routine diagnostic workup, OCCS was performed in all patients. RESULTS: 7 patients with a diagnosis of TA presented with different degrees of hypoperfusion in the CRA without hyperechoic material (referred to as "spot sign") detected by OCCS. Diagnostic workup in the remaining 17 patients revealed other causes of sudden vision loss, such as central retinal artery occlusion (CRAO) (12), anterior ischemic optic neuropathy (AION) (2), upstream vascular stenosis or occlusion (2) and delayed reperfusion of the CRA (1). The hyperechoic "spot sign" was visible in 10 of 12 patients (83 %) with embolic CRAO. The detection of embolic CRAO using the "spot sign" had a sensitivity of 83 % and a specificity of 100 %. The missing "spot sign" in patients with TA was a highly specific finding (p-value 0.01). CONCLUSION: The detection of the "spot sign" specifically minimizes the probability of TA as a reason for sudden blindness.

[Indications and outcome of ventilated patients treated in a neurological intensive care unit]. / Indikationen und Outcome beatmeter Patienten einer neurologischen Intensivstation.

OBJECTIVE: This study characterized artificially ventilated patients in a neurological intensive care unit (NICU) between 2006-2008 in a purely neurological clinic and a so-called stand-alone situation. In addition the long-term prognoses as well as the quality of life of surviving patients were investigated. METHODS: All ventilated patients from October 2006 to December 2008 were enrolled in this descriptive, retrospective study. The duration of stay in intensive care was analyzed and the current quality of life was prospectively assessed based on the patient records. Final diagnoses, duration of intensive care unit and ventilation as well as the highest score in SAPS II (simplified acute physiology score) and complications during hospitalization were determined. The patients were divided into groups based on the diagnoses as vascular, inflammatory, neurodegenerative, hereditary, epileptogenic and others. Additionally patients were contacted and asked to respond by completing questionnaires on the Barthel index (BI) and the modified Rankin scale (mRS). RESULTS: During the study period a total of 512 patients were treated in the NICU of whom 201 required artificial respiration. Cerebrovascular diseases were the main reason for therapy in the NICU in 96 out of 201 cases (47.8%), followed by inflammatory diseases in 46 (22.8%) and epileptogenic diseases in 26 patients (13%). The median duration of artificial respiration was 9 days with a mean treatment duration of 16 days (range 1-57 days). Of the patients 31 (15.4%) died in the NICU and an additional 32 patients (18.8%) died within a median of 2 months after discharge. Outcome data were available from 67 out of 170 sent questionnaires and rehabilitation reports of 86 patients, which enabled the outcome of 121 surviving patients to be analyzed (71.2%). Of these 42.2% showed no or mild impairment in everyday life. However, the remaining 38% had severe impairments according to the BI. The evaluation of the mRS showed that 49.6% of the patients still had severe symptoms. CONCLUSIONS: More than one third of the patients treated in the NICU required artificial ventilation with an emphasis on cerebrovascular diseases, which illustrates the overlap between stroke unit and NICU care. Despite a lengthy duration of ventilation and a long stay in the intensive care unit more than one third of surviving patients showed no or only mild impairment. However, an additional third suffered from severe disability up to nursing care dependency. The study data differ little from the few publications in this field despite the stand alone situation of the NICU. The case mix index per day averaged around 0.3 and underlines the economic importance with respect to other forms of neurological treatment.

Sagopilone (ZK-EPO, ZK 219477) for recurrent glioblastoma. A phase II multicenter trial by the European Organisation for Research and Treatment of Cancer (EORTC) Brain Tumor Group.

BACKGROUND: Sagopilone (ZK 219477), a lipophylic and synthetic analog of epothilone B, that crosses the blood-brain barrier has demonstrated preclinical activity in glioma models. PATIENTS AND METHODS: Patients with first recurrence/progression of glioblastoma were eligible for this early phase II and pharmacokinetic study exploring single-agent sagopilone (16 mg/m(2) over 3 h every 21 days). Primary end point was a composite of either tumor response or being alive and progression free at 6 months. Overall survival, toxicity and safety and pharmacokinetics were secondary end points. RESULTS: Thirty-eight (evaluable 37) patients were included. Treatment was well tolerated, and neuropathy occurred in 46% patients [mild (grade 1) : 32%]. No objective responses were seen. The progression-free survival (PFS) rate at 6 months was 6.7% [95% confidence interval (CI) 1.3-18.7], the median PFS was just over 6 weeks, and the median overall survival was 7.6 months (95% CI 5.3-12.3), with a 1-year survival rate of 31.6% (95% CI 17.7-46.4). Maximum plasma concentrations were reached at the end of the 3-h infusion, with rapid declines within 30 min after termination. CONCLUSIONS: No evidence of relevant clinical antitumor activity against recurrent glioblastoma could be detected. Sagopilone was well tolerated, and moderate-to-severe peripheral neuropathy was observed in despite prolonged administration.

Transcranial perfusion sonography using a low mechanical index and pulse inversion harmonic imaging: reliability, inter-/intraobserver variability.

PURPOSE: Transcranial perfusion sonography (TPS) is an emerging noninvasive bedside method for evaluating brain perfusion. The purpose was to assess the feasibility of a low MI/almost real-time frame rate approach and to test its intra-/interobserver variability. MATERIALS AND METHODS: 10 healthy volunteers were investigated 3 times with TPS at a low MI (1.0) and a high frame rate (8.3 Hz). Investigations were performed by 2 sonographers in a cross-over design: 1.) twofold measurements each with 5 volunteers (intraobserver test), and 2.) single measurements of the other 5 volunteers (interobserver test). From 8 established regions of interest (ROI), time-intensity curves (TIC) with the following parameters were calculated: peak intensity (PI), time-to-PI (TTP), area-under-curve (AUC), and cerebral transit time (CTT). The TIC quality was described by the coefficient of determination. TIC parameters were presented descriptively. Intra- and interobserver variability was tested by Spearman's correlation. RESULTS: The overall quality of the TIC was very good (mean r(2) = 0.92, 0.87 - 0.97). TTP (25.7 - 28.1 sec; mean 26.8 sec) and CTT (8.2 - 10.7 sec; mean 9.9 sec) were the most robust parameters. The intraobserver variability was lower with the more experienced sonographer (r = 0.70 vs. r = 0.29). The interobserver reliability was r = 0.34 (p < 0.05). CONCLUSION: Low MI TPS allows for nearly real-time imaging facilitating probe control. Sound sonographer experience allows for a high reliability and makes TPS an interesting tool for the diagnosis and follow-up of perfusion changes, e. g. in stroke or anti-angiogenic brain tumor therapy.

Distinct patterns of functional and structural neuroplasticity associated with learning Morse code.

Learning is based on neuroplasticity, i.e. on the capability of the brain to adapt to new experiences. Different mechanisms of neuroplasticity have been described, ranging from synaptic remodeling to changes in complex neural circuitry. To further study the relationship between changes in neural activity and changes in gray matter density associated with learning, we performed a combined longitudinal functional and morphometric magnetic resonance imaging (MRI) study on healthy volunteers who learned to decipher Morse code. We investigated 16 healthy subjects using functional MR imaging (fMRI) and voxel-based morphometry (VBM) before and after they had learned to decipher Morse code. The same set of Morse-code signals was presented to participants pre- and post-training. We found an increase in task-specific neural activity in brain regions known to be critically involved in language perception and memory, such as the inferior parietal cortex bilaterally and the medial parietal cortex during Morse code deciphering. Furthermore we found an increase in gray matter density in the left occipitotemporal region, extending into the fusiform gyrus. Anatomically neighboring sites of functional and structural neuroplasticity were revealed in the left occipitotemporal/inferior temporal cortex, but these regions only marginally overlapped. Implications of this morpho-functional dissociation for learning concepts are discussed.

Ageing abolishes the effects of fluoxetine on neurogenesis.

Depression constitutes a widespread condition observed in elderly patients. Recently, it was found that several drugs employed in therapies against depression stimulate hippocampal neurogenesis in young rodents and nonhuman primates. As the rate of neurogenesis is dramatically reduced during ageing, we examined the influences of ageing on neurogenic actions of antidepressants. We tested the impact of fluoxetine, a broadly used antidepressant, on hippocampal neurogenesis in mice of three different age groups (100, 200 and over 400 days of age). Proliferation and survival rate of newly generated cells, as well as the percentage of cells that acquired a neuronal phenotype were analyzed in the hippocampus of mice that received fluoxetine daily in a chronic manner. Surprisingly, the action of fluoxetine on neurogenesis was decreasing as a function of age and was only significant in young animals. Hence, fluoxetine increased survival and the frequency of neuronal marker expression in newly generated cells of the hippocampus in the young adult group (that is 100 days of age) only. No significant effects on neurogenesis could be detected in fluoxetine-treated adult and elderly mice (200 and over 400 days of age). The data indicate that the action of fluoxetine on neurogenesis is highly dependent on the age of the treated individual. Although the function of neurogenesis in the clinical manifestation of depression is currently a matter of speculation, this study clearly shows that the therapeutic effects of antidepressants in elderly patients are not mediated by neurogenesis modulation.

Working memory performance is correlated with local brain morphology in the medial frontal and anterior cingulate cortex in fibromyalgia patients: structural correlates of pain-cognition interaction.

Fibromyalgia (FM) is a disorder of unknown aetiology, characterized by chronic widespread pain, stiffness and sleep disturbances. In addition, patients frequently complain of memory and attention deficits. Accumulating evidence suggests that FM is associated with CNS dysfunction and with an altered brain morphology. However, few studies have specifically investigated neuropsychological issues in patients suffering from FM. We therefore sought to determine whether neuropsychological deficits found in FM patients may be correlated with changes in local brain morphology specifically in the frontal, temporal or cingulate cortices. Twenty FM patients underwent extensive testing for potential neuropsychological deficits, which demonstrated significantly reduced working memory and impaired non-verbal long-term memory (limited to free recall condition) in comparison with normative data from age- and education-matched control groups. Voxel-based morphometry (VBM) was used to evaluate for potential correlations between test results and local brain morphology. Performance on non-verbal working memory was positively correlated with grey matter values in the left dorsolateral prefrontal cortex, whereas performance on verbal working memory (digit backward) was positively correlated with grey matter values in the supplementary motor cortex. On the other hand, pain scores were negatively correlated with grey matter values in the medial frontal gyrus. White matter analyses revealed comparable correlations for verbal working memory and pain scores in the medial frontal and prefrontal cortex and in the anterior cingulate cortex. Our data suggest that, in addition to chronic pain, FM patients suffer from neurocognitive deficits that correlate with local brain morphology in the frontal lobe and anterior cingulate gyrus, which may be interpreted to indicate structural correlates of pain-cognition interaction.

[Severe tick-borne encephalomyelitis with lack of cerebrospinal fluid pleocytosis]. / Schwere Frühsommer-Meningo-Enzephalomyelitis ohne Liquor-Pleozytose.

Tick borne encephalitis (TBE) is an important viral encephalitis in central and eastern Europe. Cerebrospinal fluid (CSF) pleocytosis has been described in all published patients so far. This may be due to selection bias, however, as CSF pleocytosis is often used as a case definition parameter. The frequency of TBE without CSF pleocytosis is unknown. We report two cases who developed severe TBE without CSF pleocytosis. A normal CSF cell count should therefore not discourage from the differential diagnosis of TBE and deter from serological testing in patients with a clinical constellation suggesting TBE.

The German trial on Aciclovir and Corticosteroids in Herpes-simplex-virus-Encephalitis (GACHE): a multicenter, randomized, double-blind, placebo-controlled trial.

INTRODUCTION: Comprehensive treatment of Herpes-simplex-virus-encephalitis (HSVE) remains a major clinical challenge. The current therapy gold standard is aciclovir, a drug that inhibits viral replication. Despite antiviral treatment, mortality remains around 20% and a majority of survivors suffer from severe disability. Experimental research and recent retrospective clinical observations suggest a favourable therapy response to adjuvant dexamethasone. Currently there is no randomized clinical trial evidence, however, to support the routine use of adjuvant corticosteroid treatment in HSVE. METHODS: The German trial of Aciclovir and Corticosteroids in Herpes-simplex-virus-Encephalitis (GACHE) studied the effect of adjuvant dexamethasone versus placebo on top of standard aciclovir treatment in adult patients aged 18 up to 85 years with proven HSVE in German academic centers of Neurology in a randomized and double blind fashion. The trial was open from November 2007 to December 2012. The initially planned sample size was 372 patients with the option to increase to up to 450 patients after the second interim analysis. The primary endpoint was a binary functional outcome after 6 months assessed using the modified Rankin scale (mRS 0-2 vs. 3-6). Secondary endpoints included mortality after 6 and 12 months, functional outcome after 6 months measured with the Glasgow outcome scale (GOS), functional outcome after 12 months measured with mRS and GOS, quality of life as measured with the EuroQol 5D instrument after 6 and 12 months, neuropsychological testing after 6 months, cranial magnetic resonance imaging findings after 6 months, seizures up to day of discharge or at the latest at day 30, and after 6 and 12 months. RESULTS: The trial was stopped prematurely for slow recruitment after 41 patients had been randomized, 21 of them treated with dexamethasone and 20 with placebo. No difference was observed in the primary endpoint. In the full analysis set (n = 19 in each group), 12 patients in each treatment arm achieved a mRS of 0-2. Similarly, we did not observe significant differences in the secondary endpoints (GOS, mRS, quality of life, neuropsychological testing). CONCLUSION: GACHE being prematurely terminated demonstrated challenges encountered performing randomized, placebo-controlled trials in rare life threatening neurological diseases. Based upon our trial results the use of adjuvant steroids in addition to antiviral treatment remains experimental and is at the decision of the individual treating physician. Unfortunately, the small number of study participants does not allow firm conclusions. TRIAL REGISTRATION: EudraCT-Nr. 2005-003201-81.

Mobilization of CD34+ hematopoietic cells, colony-forming cells and long-term culture-initiating cells into the peripheral blood of patients with an acute cerebral ischemic insult.

BACKGROUND: In vitro and in vivo data indicate that stem cells found in the bone marrow (BM) are capable of differentiating into neural cells. The aim of this study was to investigate whether potentially pluripotent hematopoietic stem and progenitor cells are recruited from the BM into the peripheral blood as a reaction to ischemic damage of neural tissues. MATERIALS: The number of CD34+ cells, colony-forming cells (CFC) and long-term culture-initiating cells (LTC-IC) was measured within 24 h and on day 7 after stroke onset by flow cytometry, or in functional assays in the peripheral blood of 10 patients with acute middle cerebral artery infarct. The National Institute of Health stroke scale, Barthel index and modified Rankin scale were used to monitor the clinical outcome. RESULTS: In four patients receiving intravenous thrombolytic therapy (tissue plasminogen activator; TPA), no significant increase of CD34+ cells, CFC or LTC-IC was detected. In six patients without thrombolytic treatment, the mean number of CD34+ cells/mL increased significantly from 1181+/-248 at day 1 to 3001+/-881 at day 7. Accordingly, the numbers of CFC and LTC-IC increased 2.7- and 1.7-fold. Granulocyte colony-stimulating factor and neutrophil elastase were monitored by ELISA and remained unchanged during the study period. DISCUSSION: Our results showed a recruitment of hematopoietic progenitor cells from the BM into the peripheral blood after acute ischemic stroke when no thrombolytic treatment was given. Increased progenitor cell recruitment might be caused by so far unknown signaling stimuli of the ischemic penumbra for stem cell mobilization.

Subtle grey matter changes between migraine patients and healthy controls.

Local morphological alterations of the brain have recently been detected in cluster headache and chronic tension-type headache, but not in migraine. We investigated 35 patients suffering from migraine and compared them with 31 healthy controls with no headache history. Using magnetic resonance imaging and voxel based morphometry, we found a significant decrease of grey matter in areas ascribable to the transmission of pain (cingulate cortex), but not in areas specific for migraine, such as the brainstem. Our data are in line with recent findings in chronic pain states, such as chronic phantom pain and chronic back pain. We suggest that the grey matter change in migraine patients is the consequence of frequent nociceptive input and should thus be reversible when migraine attacks cease.

Impaired working-memory after cerebellar infarcts paralleled by changes in BOLD signal of a cortico-cerebellar circuit.

A considerable body of evidence supports the notion that cerebellar lesions lead to neuropsychological deficits, including impairments in working-memory, executive tasks and verbal fluency. Studies employing functional magnetic resonance imaging (fMRI) and anatomical tracing in primates provide evidence for a cortico-cerebellar circuitry as the functional substrate of working-memory. The present fMRI study explores the activation pattern during an n-back working-memory task in patients with an isolated cerebellar infarct. To determine each patient's cognitive impairment, neuropsychological tests of working-memory and attention were carried out. We conducted fMRI in nine patients and nine healthy age-matched controls while they performed a 2-back task in a blocked-design. In both groups we found bilateral activations in a widespread cortico-cerebellar network, consisting of the ventrolateral prefrontal cortex (BA 44, 45), dorsolateral prefrontal cortex (BA 9, 46), parietal cortex (BA 7, 40), pre-supplementary motor area (BA 6) anterior cingulate (BA 32). Relative to healthy controls, patients with isolated cerebellar infarcts demonstrated significantly more pronounced BOLD-activations in the precuneus and the angular gyrus during the 2-back task. The significant increase in activation in the posterior parietal areas of the cerebellar patients could be attributed to a compensatory recruitment to maintain task performance. We conclude that cerebellar lesions affect remote cortical regions that are part of a putative cortico-cerebellar network.

An imbalance between Smad and MAPK pathways is responsible for TGF-beta tumor promoting effects in high-grade gliomas.

The transforming growth factor-beta (TGF-beta) plays a pivotal role in the pathobiology of human gliomas: during carcinogenesis, it turns from a tumor suppressor to a tumor promoter. The traditional Smad pathway and the more recently discovered MAPK pathway are the most important pathways for TGF-beta related intracellular signal transduction mediating differential pathobiological effects. In this study, we investigated the effects of TGF-beta2 and the TGF-beta2 antisense phosphorothioate oligodeoxynucleotide (PTO) AS-11 on the functionality of both the Smad and MAPK pathways in high-grade gliomas. We aimed to correlate the imbalance between the pathways with differences in the behaviour of high-grade glioma cells. Gene and protein expression studies were used to detect levels of members of the Smad and MAPK pathways under regulation of TGF-beta2 and AS-11. Proliferation and migration assays were functional readouts for effects caused by these regulating tools. Gene arrays were used to detect yet unknown regulators of these functional effects. The Smad pathway was functional in the tested cell lines. Exogenous TGF-beta2 inhibited proliferation but enhanced migration. Smad 2 mRNA expression and activation were significantly reduced by incubation with AS-11. K-ras was reduced both in gene arrays and quPCR under treatment with AS-11, but there was no influence of K-ras down-regulation on the activity of ERK. Ubiquitination-related genes also were specifically down-regulated with AS-11. Our results indicate the involvement of K-ras in TGF-beta signaling in high-grade gliomas. ERK, which is a member of the MAPK pathway, was not influenced and seems to be activated through RAS independent cascades in glioma. These results suggest that combined antagonization of the TGF-beta and MAPK pathways might be a promising approach for glioma therapy. An imbalance between these two pathways might be responsible for TGF-beta switching to a tumor promoter protein in high-grade gliomas.

Low-dose chemotherapy in combination with COX-2 inhibitors and PPAR-gamma agonists in recurrent high-grade gliomas - a phase II study.

OBJECTIVES: Combined treatment approaches targeting tumor as well as other cells contributing to tumor progression may control chemorefractory malignancies. METHODS: A phase II trial was initiated to analyze the activity of continuously administered pioglitazone and rofecoxib combined with low-dose chemotherapy (capecitabine or temozolomide) in patients with high-grade gliomas (glioblastoma or anaplastic glioma). RESULTS: Fourteen patients were evaluable for response and toxicity. Major side effects were palmoplantar erythema, edema and motor neuropathy grade 3. Disease stabilizations lasting longer than 3 months were noted in 4 of 14 patients (29%). Clinical responses did not correspond to immunohistochemical staining for cyclooxygenase 2, peroxisome proliferator-activated receptor-gamma and CD31. DISCUSSION: The study demonstrates that this novel regimen is moderately active and well tolerated in patients with high-grade gliomas. As a comparably small proportion of patients responded, the regimen might only be suitable for a subset of highly selected patients.

The impact of white matter lesions on the cognitive outcome of subthalamic nucleus deep brain stimulation in Parkinson's disease.

OBJECTIVES: White Matter lesions (WML) are a risk factor for cognitive impairment in Parkinson's disease. There is no clear evidence of reduced general cognitive function after DBS. However, a subgroup of patients develops dementia rapidly after DBS despite careful patient selection processes. The aim of this study was to evaluate the load of WML as a possible risk factor for cognitive decline following STN DBS. PATIENTS AND METHODS: 40 PD-patients receiving bilateral STN-DBS were followed at least three years after surgery to detect dementia. All patients underwent comprehensive neuropsychological assessment and MRI before surgery. The extent of WML was assessed using an automated approach. WML volume was correlated to the onset of dementia and the decline of a cognitive composite score retrospectively. RESULTS: Patients with a rapid onset of dementia within one, respective three following DBS showed significant higher WML volumes compared to cognitive normal and MCI patients (55.8cm3±18.836 vs. 9.3cm3±12.2; p=0.002). The same significant association was found in a multivariable model, including the covariables age, gender and PD disease duration (p=0.01). WML volume was associated to the rate of decline in cognitive composite score within three years after DBS surgery (p=0.006; R2=0.40) after correction for age. CONCLUSIONS: Damaged white matter may lead to a reduced compensation of disconnections in cognitive circuits caused by the implantation of the DBS electrodes or by chronic stimulation. The role of WML as a prognostic factor for the cognitive outcome after DBS may be underestimated. The WML burden should be taken seriously in preoperative risk stratification.

Calcified neurocysticercosis lesions trigger symptomatic inflammation during antiparasitic therapy.

We report a patient with neurocysticercosis who developed numerous cerebral edematous lesions while undergoing cysticidal therapy. These lesions outnumbered viable cystic lesions seen before therapy. Most new lesions were subsequently found to be associated with former calcifications not seen on initial MR imaging. Calcified neurocysticercosis lesions can trigger inflammatory reactions during therapy, and the number and location of calcified neurocysticercosis lesions may influence treatment decisions.

In vivo high-resolution MR imaging of neuropathologic changes in the injured rat spinal cord.

BACKGROUND AND PURPOSE: MR imaging is the most comprehensive noninvasive means to assess structural changes in injured central nervous system (CNS) tissue in humans over time. The few published in vivo MR imaging studies of spinal cord injury in rodent models by using field strengths < or = 7T suffer from low spatial resolution, flow, and motion artifacts. The aim of this study was to assess the capacity of a 17.6T imaging system to detect pathologic changes occurring in a rat spinal cord contusion injury model ex vivo and in vivo. METHODS: Seven adult female Fischer 344 rats received contusion injuries at thoracic level T10, which caused severe and reproducible lesions of the injured spinal cord parenchyma. Two to 58 days postinjury, high-resolution MR imaging was performed ex vivo (2) or in vivo in anesthetized rats (5 spinal cord injured + one intact control animal) by using 2D multisection spin- and gradient-echo imaging sequences, respectively, combined with electrocardiogram triggering and respiratory gating. RESULTS: The acquired images provided excellent resolution and gray/white matter differentiation without significant artifacts. Signal intensity changes, which were detected with ex vivo and in vivo MR imaging following spinal cord injury, could be correlated with histologically defined structural changes such as edema, fibroglial scar, and hemorrhage. CONCLUSIONS: These results demonstrate that MR imaging at 17.6T allows high-resolution structural analysis of spinal cord pathology after injury.