Normalized serum eosinophil peroxidase levels are inversely correlated with esophageal eosinophilia in eosinophilic esophagitis.

Eosinophil peroxidase is an eosinophil-specific, cytoplasmic protein stored in the secondary granules of eosinophils. While eosinophil peroxidase deposition is increased in the esophagus in eosinophilic esophagitis (EOE), its potential role as a peripheral marker is unknown. This study aims to examine the relationship between serum eosinophil peroxidase and esophageal eosinophilia in eosinophilic esophagitis. Prospectively collected serum from 19 subjects with incident EoE prior to treatment and 20 non-EoE controls were tested for serum eosinophil peroxidase, eosinophilic cationic protein, and eosinophil derived neurotoxin using ELISA. Matching esophageal tissue sections were stained and assessed for eosinophil peroxidase deposition using a histopathologic scoring algorithm. Mean peripheral blood absolute eosinophil counts in eosinophilic esophagitis subjects were significantly elevated compared to controls (363 vs. 195 cells/µL, P = 0.008). Absolute median serum eosinophil peroxidase, eosinophil cationic protein, and eosinophil derived neurotoxin did not differ between groups; however, when normalized for absolute eosinophil counts, eosinophilic esophagitis subjects had significantly lower median eosinophil peroxidase levels (2.56 vs. 6.96 ng/mL per eos/µL, P = 0.002, AUC 0.79 (0.64, 0.94 95% CI)). Multivariate analysis demonstrated this relationship persisted after controlling for atopy. Esophageal biopsies from eosinophilic esophagitis subjects demonstrated marked eosinophil peroxidase deposition (median score 46 vs. 0, P < 0.0001). Normalized eosinophil peroxidase levels inversely correlated with esophageal eosinophil density (r = -0.41, P = 0.009). In contrast to marked tissue eosinophil degranulation, circulating eosinophils appear to retain their granule proteins in EoE. Investigations of normalized serum eosinophil peroxidase levels as a biomarker of EoE are ongoing.

Single-Layer WEBs: Intrasaccular Flow Disrupters for Aneurysm Treatment­Feasibility Results from a European Study.

BACKGROUND AND PURPOSE: The safety and efficiency of the dual-layer Woven EndoBridge (WEB) device has already been published. However, this international multicenter study sought to evaluate the safety of single-layer devices, which are the newest generation of the WEB intrasaccular flow-disrupter family. They have been designed to offer smaller-sized devices with a lower profile to optimize navigability and delivery, which may, in turn, broaden their range of use. MATERIALS AND METHODS: Data from all consecutive patients treated with a single-layer WEB device, in 10 European centers from June 2013 to May 2014 were included. Clinical presentations, technical details, intra- and perioperative complications, and outcomes at discharge were recorded. Clinical and angiographic data at last follow-up were also analyzed when available. RESULTS: Ninety patients with 98 WEB-treated aneurysms were included in this study. In 93 cases (95%), WEB placement was possible. Complete occlusion at the end of the procedure was obtained in 26 instances (26%). Additional treatment during the procedure (coiling and/or stent placement) was necessary in 12 cases (12.7%). Procedure-related complications occurred in 13 cases, leading to permanent neurologic deficits in 4 patients (4.4%). Early vascular imaging follow-up data were available for 44 patients (57%), with an average time interval of 3.3 months. Treatment-related morbidity and mortality rates at last follow-up were 2.2% and 1.1%, respectively. CONCLUSIONS: In this study, the feasibility and safety of the single-layer WEB device was comparable with that of the double-layer. However, further studies are needed to evaluate long-term efficacies.

Differential activation of airway eosinophils induces IL-13-mediated allergic Th2 pulmonary responses in mice.

BACKGROUND: Eosinophils are hallmark cells of allergic Th2 respiratory inflammation. However, the relative importance of eosinophil activation and the induction of effector functions such as the expression of IL-13 to allergic Th2 pulmonary disease remain to be defined. METHODS: Wild-type or cytokine-deficient (IL-13(-/-) or IL-4(-/-) ) eosinophils treated with cytokines (GM-CSF, IL-4, IL-33) were adoptively transferred into eosinophil-deficient recipient mice subjected to allergen provocation using established models of respiratory inflammation. Allergen-induced pulmonary changes were assessed. RESULTS: In contrast to the transfer of untreated blood eosinophils to the lungs of recipient eosinophil deficient mice, which induced no immune/inflammatory changes either in the lung or in the lung draining lymph nodes (LDLN), pretreatment of blood eosinophils with GM-CSF prior to transfer elicited trafficking of these eosinophils to LDLN. In turn, these LDLN eosinophils elicited the accumulation of dendritic cells and CD4(+) T cells to these same LDLNs without inducing pulmonary inflammation. However, exposure of eosinophils to GM-CSF, IL-4, and IL-33 prior to transfer induced not only immune events in the LDLN, but also allergen-mediated increases in airway Th2 cytokine/chemokine levels, the subsequent accumulation of CD4(+) T cells as well as alternatively activated (M2) macrophages, and the induction of pulmonary histopathologies. Significantly, this allergic respiratory inflammation was dependent on eosinophil-derived IL-13, whereas IL-4 expression by eosinophils had no significant role. CONCLUSION: The data demonstrate the differential activation of eosinophils as a function of cytokine exposure and suggest that eosinophil-specific IL-13 expression by activated cells is a necessary component of the subsequent allergic Th2 pulmonary pathologies.

Case report: a troublesome ophthalmic artery aneurysm.

Objective and Importance When treating large unruptured ophthalmic artery (OA) aneurysms causing progressive blindness, surgical clipping is still the preferred method because aneurysm sac decompression may relieve optic nerve compression. However, endovascular treatment of OA aneurysms has made important progress with the introduction of stents. Although this development is welcomed, it also makes the choice of treatment strategy less straightforward than in the past, with the potential of missteps. Clinical Presentation A 56-year-old woman presented with a long history of progressive unilateral visual loss and magnetic resonance imaging showing a 20-mm left-sided OA aneurysm. Intervention Because of her long history of very poor visual acuity, we considered her left eye to be irredeemable and opted for endovascular therapy. The OA aneurysms was treated with stent and coils but continued to grow, threatening the contralateral eye. Because she failed internal carotid artery (ICA) balloon test occlusion, we performed a high-flow extracranial-intracranial bypass with proximal ICA occlusion in the neck. However, aneurysm growth continued due to persistent circulation through reversed blood flow in distal ICA down to the OA and the cavernous portion of the ICA. Due to progressive loss of her right eye vision, we surgically occluded the ICA proximal to the posterior communicating artery and excised the coiled, now giant, OA aneurysm. This improved her right eye vision, but her left eye was permanently blind. Conclusion This case report illustrates complications of the endovascular and surgical treatment of a large unruptured OA aneurysm.

Re-defining the unique roles for eosinophils in allergic respiratory inflammation.

The role of eosinophils in the progression and resolution of allergic respiratory inflammation is poorly defined despite the commonality of their presence and in some cases their use as a biomarker for disease severity and/or symptom control. However, this ambiguity belies the wealth of insights that have recently been gained through the use of eosinophil-deficient/attenuated strains of mice that have demonstrated novel immunoregulatory and remodelling/repair functions for these cells in the lung following allergen provocation. Specifically, studies of eosinophil-deficient mice suggest that eosinophils contribute to events occurring in the lungs following allergen provocation at several key moments: (i) the initiating phase of events leading to Th2-polarized pulmonary inflammation, (ii) the suppression Th1/Th17 pathways in lung-draining lymph nodes, (iii) the recruitment of effector Th2 T cells to the lung, and finally, (iv) mechanisms of inflammatory resolution that re-establish pulmonary homoeostasis. These suggested functions have recently been confirmed and expanded upon using allergen provocation of an inducible eosinophil-deficient strain of mice (iPHIL) that demonstrated an eosinophil-dependent mechanism(s) leading to Th2 dominated immune responses in the presence of eosinophils in contrast to neutrophilic as well as mixed Th1/Th17/Th2 variant phenotypes in the absence of eosinophils. These findings highlighted that eosinophils are not exclusively downstream mediators controlled by T cells, dendritic cells (DC) and/or innate lymphocytic cells (ILC2). Instead, eosinophils appear to be more aptly described as significant contributors in complex interrelated pathways that lead to pulmonary inflammation and subsequently promote resolution and the re-establishment of homoeostatic baseline. In this review, we summarize and put into the context the evolving hypotheses that are now expanding our understanding of the roles eosinophils likely have in the lung following allergen provocation.

Eosinophil activities modulate the immune/inflammatory character of allergic respiratory responses in mice.

BACKGROUND: The importance and specific role(s) of eosinophils in modulating the immune/inflammatory phenotype of allergic pulmonary disease remain to be defined. Established animal models assessing the role(s) of eosinophils as contributors and/or causative agents of disease have relied on congenitally deficient mice where the developmental consequences of eosinophil depletion are unknown. METHODS: We developed a novel conditional eosinophil-deficient strain of mice (iPHIL) through a gene knock-in strategy inserting the human diphtheria toxin (DT) receptor (DTR) into the endogenous eosinophil peroxidase genomic locus. RESULTS: Expression of DTR rendered resistant mouse eosinophil progenitors sensitive to DT without affecting any other cell types. The presence of eosinophils was shown to be unnecessary during the sensitization phase of either ovalbumin (OVA) or house dust mite (HDM) acute asthma models. However, eosinophil ablation during airway challenge led to a predominantly neutrophilic phenotype (>15% neutrophils) accompanied by allergen-induced histopathologies and airway hyper-responsiveness in response to methacholine indistinguishable from eosinophilic wild-type mice. Moreover, the iPHIL neutrophilic airway phenotype was shown to be a steroid-resistant allergic respiratory variant that was reversible upon the restoration of peripheral eosinophils. CONCLUSIONS: Eosinophil contributions to allergic immune/inflammatory responses appear to be limited to the airway challenge and not to the sensitization phase of allergen provocation models. The reversible steroid-resistant character of the iPHIL neutrophilic airway variant suggests underappreciated mechanisms by which eosinophils shape the character of allergic respiratory responses.

Clinical implications of internal carotid artery flow impairment caused by filter occlusion during carotid artery stenting.

BACKGROUND AND PURPOSE: Membrane filters are EPDs, which preserve ICA flow during CAS. However, ICA flow arrest may occur with filter use. This report describes the angiographic, clinical, and histopathologic features of the filter occlusion. MATERIALS AND METHODS: Sixty-one consecutive patients with cervical carotid stenosis treated by CAS by using a single type of filter device were evaluated. All patients were on dual antiplatelet treatment and fully heparinized. Prestent dilation was performed in all patients. Poststent dilation was performed in 15 patients. Control angiograms were obtained and evaluated after each step of the CAS procedure. All filters were inspected for debris, and if present, histology was obtained. RESULTS: CAS was successfully performed in all cases with <20% residual stenosis. Filter occlusion occurred in 6 patients (9.8%). It developed immediately after stent deployment in 4, and after a second prestent dilation in 2. Five of the 6 had severe carotid stenosis. In all patients, filter withdrawal led to immediate and complete restoration of ICA flow. In 1 patient, acute embolic M1 occlusion occurred immediately after filter withdrawal but was successfully treated with thrombolysis. None of filter-occlusion group had permanent neurologic deficits. Gross and microscopic examinations demonstrated that the pores of the filters were occluded mainly by fibrin. Postoperative diffusion MR imaging revealed no difference between filter-occlusion and non-filter-occlusion groups. CONCLUSIONS: ICA flow arrest due to filter occlusion during CAS is relatively common and occurs more frequently in severe stenosis. It resolves rapidly after filter removal and does not appear to worsen outcome.

Eosinophils in health and disease: the LIAR hypothesis.

Discussions of eosinophils are often descriptions of end-stage effector cells with destructive capabilities mediated predominantly by released cytotoxic cationic granule proteins. Moreover, eosinophils in the medical literature are invariably associated with the pathologies linked with helminth infections or allergic diseases such as asthma. This has led to an almost fatalist view of eosinophil effector functions and associated therapeutic strategies targeting these cells that would make even William of Ockham proud - eosinophil effector functions have physiological consequences that increase patient morbidity/mortality and 'the only good eosinophils are dead eosinophils'. Unfortunately, the strengths of dogmas are also their greatest weaknesses. Namely, while the repetitive proclamation of dogmatic concepts by authoritative sources (i.e. reviews, meeting proceedings, textbooks, etc.) builds consensus within the medical community and lower the entropies surrounding difficult issues, they often ignore not easily explained details and place diminished importance on alternative hypotheses. The goal of this perspective is twofold: (i) we will review recent observations regarding eosinophils and their activities as well as reinterpret earlier data as part of the synthesis of a new paradigm. In this paradigm, we hypothesize that eosinophils accumulate at unique sites in response to cell turnover or in response to local stem cell activity(ies). We further suggest that this accumulation is part of one or more mechanisms regulating tissue homeostasis. Specifically, instead of immune cells exclusively mediating innate host defence, we suggest that accumulating tissue eosinophils are actually regulators of Local Immunity And/or Remodeling/Repair in both health and disease - the LIAR hypothesis; (ii) we want to be inflammatory (pun intended!) and challenge the currently common perspective of eosinophils as destructive end-stage effector cells. Our hope is to create more questions than we answer and provoke everyone to spend countless hours simply to prove us wrong!

Introduction of endovascular embolization for intracranial aneurysms in a low-volume institution.

BACKGROUND: Studies indicate a relationship between hospital caseload and health outcomes after both surgical and endovascular repair of intracranial aneurysms. PURPOSE: To evaluate outcomes after introduction of endovascular embolization for intracranial aneurysms in a low-volume regional university hospital. MATERIAL AND METHODS: Retrospective study of 243 consecutive patients treated for 284 intracranial aneurysms with endovascular embolization or surgical clipping from 2000 to 2006 at the University Hospital of North Norway. Postoperative complications were registered. The Glasgow Outcome Scale (GOS) was used for assessment of outcome. RESULTS: The mean annual number of procedures was 39 (microsurgery 23, embolization 16). Seventy-four percent of patients with ruptured aneurysms and all patients with unruptured aneurysms had a favorable outcome (GOS 4 or 5) at 1 year follow-up. Patients with subarachnoid hemorrhage were more likely to experience postoperative complications than patients treated for unruptured aneurysms (42% versus 8% of the patients, P<0.01). The immediate incomplete occlusion rate (Raymond II-III) in the initial embolization procedure was 29%. Ten endovascularly treated patients and one surgically treated patient required retreatments due to residual aneurysm or neck remnants. CONCLUSION: The present study indicates that acceptable outcome from aneurysm treatment, both endovascular and microsurgical, is possible in a low-volume institution.

Gliosarcoma with liposarcomatous component, bone infiltration and extracranial growth.

Gliosarcoma is a highly malignant brain tumor consisting of both a glioblastoma and a mesenchymal component. The latter typically resembles fibrosarcoma, but differentiation patterns resembling osteosarcoma, chondrosarcoma, angiosarcoma and rhabdomyosarcoma have also been described. Molecular-genetic studies have shown that both glioblastoma and the mesenchymal component share identical cytogenetic abnormalities or mutations, suggesting a monoclonal origin from glial cells. We report an unusual case of gliosarcoma that presented as a large intracerebral tumor with infiltration of the temporal bone and the soft tissues in the infratemporal fossa. Microscopically, the tumor consisted of alternating areas of glioblastoma and fibrosarcoma. Focally, areas ofosteosarcomatous and liposarcomatous differentiation were found. Although gliosarcoma with transcranial penetration is very rare, it should be suspected in case of intracranial tumor with glioblastoma-imaging features, infiltration of bone and extracranial growth. Our case of liposarcomatous differentiation in gliosarcoma--together with another very recently reported similar case--expands the morphologic heterogeneity of this peculiar brain tumor.

Detection of cerebral embolic signals in patients with systemic lupus erythematosus.

BACKGROUND: Involvement of the CNS in systemic lupus erythematosus (SLE) is caused by several pathogenic mechanisms including cerebral embolism. AIM: To measure the frequency of microembolic signals (MES) by using transcranial Doppler (TCD) ultrasound and to assess their association with cerebral infarction, neuropsychological dysfunction, and biochemical, sonographic and clinical variables in an unselected group of patients with SLE. METHODS: A 1-h TCD recording from the middle cerebral artery was carried out in 55 patients with SLE having a mean age of 46 (SD 13) years. MRI of the brain, carotid artery ultrasonography with intima-media thickness and atherosclerotic plaque assessments were carried out in addition to a broad biochemical and clinical assessment. All patients underwent a neuropsychological assessment. RESULTS: Of the 55 patients, MES were detected in 5 (9%) and cerebral infarcts were found in 9 (18%). A significant association was found between MES and cerebral infarcts and considerably more neuropsychological deficits were found in MES-positive patients compared with the negative group. MES were not associated with other clinical, sonographic and biochemical factors believed to be associated with cerebral embolism. CONCLUSIONS: Cerebral embolism may be one of the important mechanisms responsible for the high prevalence of cerebrovascular events and the neuropsychological deficits observed in patients with SLE. Although the number of MES-positive patients was small, the lack of a significant association between MES and other known risk factors for MES suggests a complex pathogenesis for the embolisation in these patients.

Pulmonary function and high-resolution CT findings five years after disease onset in patients with Wegener's granulomatosis.

OBJECTIVE: Although pulmonary involvement is common in Wegener's granulomatosis (WG), little is known about the pulmonary outcome. We evaluated the relationship between clinical disease characteristics and pulmonary function and high-resolution computed tomography (HRCT) findings after disease duration of 5 years. METHODS: A pulmonary function test (PFT) and pulmonary HRCT were performed in 41 patients from a population-based register of WG. Clinical predictors for abnormal PFT and HRCT were tested by logistic regression. RESULTS: Previous WG-related lung involvement (PLI) had occurred in 80% of patients, but only 24% of patients still reported pulmonary symptoms at the research visit. One-third of patients had abnormal PFT findings, with reduced alveolar diffusion by KCO (transfer coefficient) being most common (24%). The number of PLI episodes was associated with reduced KCO and reduced FEV1% (forced expiratory volume in 1 s as a percentage of forced vital capacity) (overall presence 10%). Reduced KCO was also associated with disease duration. Reduced total lung capacity (TLC) (overall presence 8%) was only related to prior WG-related lung nodules. Pulmonary HRCT was abnormal in 80%, but with more severe abnormalities in only 30%. Pleural thickening and parenchymal bands were associated with PLI. None of the treatment variables was associated with the PFT or HRCT findings. CONCLUSION: Five years after disease onset a quarter of the WG patients reported pulmonary symptoms, had severe abnormalities on HRCT, and abnormal PFT. The correlation between these abnormalities was poor, but the number of pulmonary involvements was a risk factor for reduced gas diffusion, obstructive lung disease, parenchymal bands, and pleural thickening. Treatment variables had no discernible negative pulmonary effects.

Outcome 1 year after aneurysmal subarachnoid hemorrhage: relation between cognitive performance and neuroimaging.

OBJECTIVE: To assess the cognitive impairment and the association between neuropsychological measures and neuroimaging 1 year after aneurysmal subarachnoid hemorrhage (SAH). METHOD: Forty-two patients were examined clinically according to Glasgow Outcome Scale (GOS). Computed tomography (CT), single photon emission computed tomography (SPECT) and neuropsychological examination were performed. RESULTS: There were no association between GOS and cognitive impairment index based on the neuropsychological examination. CT showed no sign of cerebral ischemia in 17 (40%) and low attenuating areas indicating cerebral infarction(s) in 25 (60%) patients. A significant correlation (P = 0.01) was observed between the cognitive impairment index and the SPECT index (r = 0.6). SPECT measurement was the only independent predictor for cognitive impairment. CONCLUSION: GOS is a crude outcome measure and patients classified with good recoveries may have significant cognitive deficits. Neuropsychological examination is the preferred method for outcome evaluation as this method specifically addresses the disabilities affecting patients' everyday life.

Reduced neuropsychological test performance in asymptomatic carotid stenosis: The Tromsø Study.

OBJECTIVE: To assess the relationship between asymptomatic carotid stenosis, neuropsychological test performance, and silent MRI lesions. METHODS: Performance on several neuropsychological tests was compared in 189 subjects with ultrasound-assessed carotid stenosis and 201 control subjects without carotid stenosis, recruited from a population health study. Subjects with a previous history of stroke were excluded. The test battery included tests of attention, psychomotor speed, memory, language, speed of information processing, motor functioning, intelligence, and depression. Sagittal T1-weighted and axial and coronal T2-weighted spin echo MRI was performed, and presence of MRI lesions (white matter hyperintensities, lacunar and cortical infarcts) was recorded. RESULTS: Subjects with carotid stenosis had significantly lower levels of performance in tests of attention, psychomotor speed, memory, and motor functioning, independent of MRI lesions. There were no significant differences in tests of speed of information processing, word association, or depression. Cortical infarcts and white matter hyperintensities were equally distributed among persons with and without carotid stenosis. Lacunar infarcts were more frequent in the stenosis group (p = 0.03). CONCLUSIONS: Carotid stenosis was associated with poorer neuropsychological performance. This could not be explained by a higher proportion of silent MRI lesions in persons with asymptomatic carotid stenosis, making it less likely that the cognitive impairment was caused by silent emboli.

Neuropsychological dysfunction in systemic lupus erythematosus is not associated with changes in cerebral blood flow.

Cognitive dysfunction is found in a considerable proportion of patients with systemic lupus erythematosus (SLE). SPECT provides an estimate of regional cerebral blood flow (rCBF) which has been claimed to be sensitive to detect brain involvement in SLE. It is, however, uncertain if these perfusion defects are related to cognitive dysfunction. In the present study we investigated whether cerebral dysfunction assessed by neuropsychological measures was associated with changes in rCBE Fifty-two SLE patients were examined with a battery of neuropsychological tests and MRI of the brain. For each patient 99mTC-HMPAO-SPECT was performed with the visual cortex as reference, and a reduction in rCBF of > 15% was considered abnormal. Regional CBF was performed with an automated computer program quantitatively estimating blood perfusion in 16 symmetrical sectors of the brain. Several sectors of the brain showed varying areas of reduced rCBF with the temporal lobes most frequently involved. There were generally no associations between cognitive level of functioning and reduced rCBF. MRI demonstrated cerebral infarcts in 9 (17%) patients. In general rCBF was reduced in all sectors of the brain in patients with infarcts, although statistical significant difference in rCBF between patients with and without infarcts was only seen in the parietal lobe. Several neuropsychological functions were influenced by the presence of cerebral infarcts. There was no significant association between immunological measures and SPECT findings or neuropsychological measures. Neuropsychological dysfunction in SLE was associated with the presence of cerebral infarcts detected by MRI, but not by changes in rCBF. SPECT seems to add little if any information to that obtained by clinical examination, neuropsychological testing, and MRI. Since anticoagulation may prevent cerebral infarcts, such prophylactic intervention may be of importance in preventing cognitive deterioration.

MRI of cervical spine with flexion and extension used in patients with rheumatoid arthritis.

Patients with rheumatoid arthritis (RA) often have involvement of the cervical spine. The most common abnormality is atlanto-axial subluxation (AAS). The more serious vertical subluxation (VS) is thought to develop at a later stage. Direct cord compression may occur, but the symptoms may be vague and difficult to interpret. In addition to clinical follow up, RA patients undergo several conventional radiographs of the cervical spine, with addition of flexion and extension images. This, in spite of the fact that the cervical cord and soft tissue do not show. Magnetic resonance imaging (MRI), is the modality of choice to visualize soft tissue and the cervical medulla, but is rarely performed in the follow up of RA patients. Five patients with long-standing RA, episodes of neck pain, and known AAS were asked to volunteer for a MRI study of the cervical spine, consisting of sagittal T2 weighted images of the cervical spine during flexion and extension of the neck. Compared to clinical examinations and cervical radiographs, MRI gave valuable information not otherwise obtained. The importance of MRI with the neck in a flexed and extended position is stressed. This is possible to obtain within a conventional quadrature neck coil in many RA patients.

Imaging findings in schwannomas of the jugular foramen.

BACKGROUND AND PURPOSE: Tumors of the cranial nerve sheath constitute 5% to 10% of all intracranial neoplasms, yet few articles have described their CT and MR characteristics. We report the imaging findings in a relatively large series of schwannomas of the jugular foramen, contrasting them with other disease entities, especially vestibular schwannomas and tumors of the glomus jugulare. METHODS: CT and/or MR studies of eight patients who underwent surgery for histologically proved schwannomas were reviewed retrospectively. One additional patient with an assumed schwannoma of the jugular foramen, who did not have surgery, was also included. RESULTS: Surgical findings showed schwannomas of the glossopharyngeal nerve in seven patients and tumor involvement of both the glossopharyngeal and vagal nerves in one patient. All tumors were partially located within the jugular foramen. Growth extending within the temporal bone was typical. Tumor extended into the posterior cranial fossa in all nine patients and produced mass effect on the brain stem and/or cerebellum in seven patients; in five patients, tumor extended below the skull base. On unenhanced CT scans, tumors were isodense with brain in six patients and hypodense in two. In seven patients, CT scans with bone algorithm showed an enlarged jugular foramen with sharply rounded bone borders and a sclerotic rim. On MR images, T1 signal from tumor was low and T2 signal was high relative to white matter in all patients. Contrast enhancement on CT and/or MR studies was strong in eight patients and moderate in one. CONCLUSION: Schwannoma of the jugular foramen is characteristically a sharply demarcated, contrast-enhancing tumor, typically centered on or based in an enlarged jugular foramen with sharply rounded bone borders and a sclerotic rim. Intraosseous extension may be marked.

Postoperative nerve root displacement and scar tissue. A prospective cohort study with contrast-enhanced MR imaging one year after microdiscectomy.

PURPOSE: To investigate the association between postoperative nerve root displacement and epidural scar tissue. MATERIAL AND METHODS: One hundred patients who had undergone lumbar microdiscectomy were included in a prospective cohort study with a 1-year follow-up. The patients were classified as failures or successes at the 12-month follow-up according to a clinical score. Patients with signs of recurrent disc herniation on MR were excluded from the study. All the 13 patients classified as failures were investigated with MR at the 1-year follow-up, and 40 patients classified as successes were picked at random for MR imaging; thus MR was performed in 53 patients. The MR images were independently evaluated by two neuroradiologists. The images were rated according to the presence or absence of nerve root displacement at the surgically treated disc interspace. Scar formation was rated according to two different classification systems. RESULTS: Nerve root displacement was observed in 13 patients. No evidence of scar formation was found in 4 patients, a small amount in 11, intermediate in 37 and extensive scar formation in 1 patient. No association between nerve root displacement and the amount of scar tissue was found. CONCLUSION: Postoperative nerve root displacement seems to be an independent clinical entity not associated to postoperative scar tissue.

Traumatic brain damage in minor head injury: relation of serum S-100 protein measurements to magnetic resonance imaging and neurobehavioral outcome.

OBJECTIVE: The present study was conducted to validate S-100 protein as a marker of brain damage after minor head injury. METHODS: We studied 50 patients with minor head injuries and Glasgow Coma Scale scores of 13 to 15 in whom computed tomographic scans of the brain revealed no abnormalities. Serum levels of S-100 protein were measured at admittance and hourly thereafter until 12 hours after injury. Magnetic resonance imaging and baseline neuropsychological examinations were performed within 48 hours, and neuropsychological follow-up was conducted at 3 months postinjury. RESULTS: Fourteen patients (28%) had detectable serum levels of S-100 protein (mean peak value, 0.4 microg/L [standard deviation, +/- 0.3]). The S-100 protein levels were highest immediately after the trauma, and they declined each hour thereafter. At 6 hours postinjury, the serum level was below the detection limit (0.2 microg/L) in five (36%) of the patients with initially detectable levels. Magnetic resonance imaging revealed brain contusions in five patients, four of whom demonstrated detectable levels of S-100 protein in serum. The proportion of patients with detectable serum levels was significantly higher when magnetic resonance imaging revealed a brain contusion. In patients with detectable serum levels, we observed a trend toward impaired neuropsychological functioning on measures of attention, memory, and information processing speed. CONCLUSION: Determination of S-100 protein levels in serum provides a valid measure of the presence and severity of traumatic brain damage if performed within the first hours after minor head injury.

Cerebral computed tomography and electroencephalography compared with neuropsychological findings in systemic lupus erythematosus.

Central nervous system involvement was evaluated in 36 patients with systemic lupus erythematosus (SLE) using cerebral computed tomography (CT), electroencephalography (EEG), and a neuropsychological test battery. The purpose was to investigate whether brain dysfunction as assessed by comprehensive neuropsychological investigation is associated with findings of routine investigation methods such as CT and EEG which are available in most hospitals. Abnormal EEG was found in 19%, and CT revealed cerebral atrophy in 47% of SLE patients. Few neuropsychological functions were affected by the presence of abnormal EEG, cerebral atrophy, or infarcts. Significant associations were found only between cortical atrophy and impairment of tactile spatial problem-solving and motor dexterity, and between cortical infarcts and motor dexterity in the dominant hand. The value of conventional EEG in assessing cerebral SLE is negligible, except for identifying epileptic activity and focal pathology. Cerebral CT has little relevance in predicting brain dysfunction as established by neuropsychological assessment in SLE, except for detecting cortical atrophy and infarcts.