Affective Symptoms and White Matter Changes in Brain Tumor Patients.

BACKGROUND: Affective symptoms are frequent in patients with brain tumors. The origin of such symptoms is unknown; either focal brain injury or reactive emotional distress may be responsible. This cross-sectional pilot study linked depressive symptoms and anxiety to white matter integrity. The objective was to test the hypothesis of a relationship between tissue damage and brain function in patients with brain tumors and to provide a basis for further studies in this field. METHODS: Diffusion tensor imaging was performed in 39 patients with newly diagnosed supratentorial primary brain tumor. Patients completed the Beck Depression Inventory, and examiners rated them on the Hamilton Depression Rating Scale (HDRS). State and trait anxiety were measured using the State-Trait Anxiety Inventory. Correlations between fractional anisotropy (FA) and psychological measures were assessed on the basis of regions of interest; the defined regions of interest corresponded to clearly specified white matter tracts. RESULTS: Statistical analysis revealed correlations between FA in the left internal capsule and scores on the HDRS, Beck Depression Inventory, and State-Trait Anxiety Inventory (P < 0.05). HDRS scores were also correlated with FA in the right medial uncinate fasciculus, and state anxiety scores were significantly correlated with FA in the left lateral and medial uncinate fasciculus (P < 0.05). CONCLUSIONS: Our results suggest that neurobiologic mechanisms related to the integrity of tissue in specific white matter tracts may influence affective symptoms in patients with brain tumors, and these mechanisms can be investigated with diffusion tensor imaging. However, prospective observational studies are needed to investigate further the links between brain structures and the severity of affective symptoms in this patient population.

In vivo quantification of cerebral r2*-response to graded hyperoxia at 3 tesla.

OBJECTIVES: This study aims to quantify the response of the transverse relaxation rate of the magnetic resonance (MR) signal of the cerebral tissue in healthy volunteers to the administration of air with step-wise increasing percentage of oxygen. MATERIALS AND METHODS: The transverse relaxation rate (R2*) of the MR signal was quantified in seven volunteers under respiratory intake of normobaric gas mixtures containing 21, 50, 75, and 100% oxygen, respectively. End-tidal breath composition, arterial blood saturation (SaO2), and heart pulse rate were monitored during the challenge. R2* maps were computed from multi-echo, gradient-echo magnetic resonance imaging (MRI) data, acquired at 3.0T. The average values in the segmented white matter (WM) and gray matter (GM) were tested by the analysis of variance (ANOVA), with Bonferroni post-hoc correction. The GM R2*-reactivity to hyperoxia was modeled using the Hill's equation. RESULTS: Graded hyperoxia resulted in a progressive and significant (P < 0.05) decrease of the R2* in GM. Under normoxia the GM-R2* was 17.2 ± 1.1 s(-1). At 75% O2 supply, the R2* had reached a saturation level, with 16.4 ± 0.7 s(-1) (P = 0.02), without a significant further decrease for 100% O2. The R2*-response of GM correlated positively with CO2 partial pressure (R = 0.69 ± 0.19) and negatively with SaO2 (R = -0.74 ± 0.17). The WM showed a similar progressive, but non-significant, decrease in the relaxation rates, with an increase in oxygen intake (P = 0.055). The Hill's model predicted a maximum R2* response of the GM, of 3.5%, with half the maximum at 68% oxygen concentration. CONCLUSIONS: The GM-R2* responds to hyperoxia in a concentration-dependent manner, suggesting that monitoring and modeling of the R2*-response may provide new oxygenation biomarkers for tumor therapy or assessment of cerebrovascular reactivity in patients.

Enchondroma of the nasal septum due to Ollier disease: a case report and review of the literature.

BACKGROUND: Morbus Ollier is characterized by the presence of multiple enchondromas (ie, benign intraosseous cartilaginous lesions). Although their manifestation in the limb bones is well described, only a few cases with ear, nose, and throat (ENT) involvement, primarily arising from the skull, have been reported. The malignant transformation toward slowly growing low-grade chondrosarcomas is the most severe form of progression. METHODS: We report a unique case of a 54-year-old patient with Ollier disease with an extensive nasal enchondroma apparently eroding the middle nasal concha and expanding to the lateral nasal wall that raised suspicion of malignant transformation. RESULTS: Radiological and histological features of enchondromas can be controversial and seem to have limited sensitivity to exclude low-grade malignancy. The clinical symptoms play a decisive role in differentiation between enchondromas and low-grade chondrosarcomas. CONCLUSION: Surgery remains the only effective solution in removing an enchondroma and preventing the tendency toward malignant transformation.

Acute necrotizing encephalopathy (ANE1): rare autosomal-dominant disorder presenting as acute transverse myelitis.

The term "acute transverse myelitis (ATM)" comprises various non-traumatic disorders that eventually can be associated with a focal myelopathy. Patients characteristically present with an acutely occurring paraparesis/plegia and require a comprehensive and timely diagnostic work up for the initiation of an appropriate treatment. We present a case of a 36-year-old female patient with a rare genetic disorder (ANE1: Acute Necrotizing Encephalopathy due to a RANBP2 mutation) who presented with an acute quadriplegia. Following an acute pulmonal infection, she rapidly (< 24 h) developed a severe quadriplegia (total motor score 38) with some facial sensory symptoms (perioral hypoesthesia). Magnetic resonance imaging (MRI) revealed a combination of longitudinal extensive transverse myelitis and symmetrical thalamic lesions. A work-up for infectious and systemic diseases was negative; specifically, no findings related to multiple sclerosis, neuromyelitis optica or vascular disorders. After empirical high dose steroid treatment and rehabilitation therapy, the patient gained almost normal gait and upper limb function. She was found to carry an autosomal-dominant missense mutation in the RANBP2 gene predisposing for ANE. Gene segregation was confirmed in other family members that had been affected by other episodes of acute steroid-responsive encephalopathies. We propose that a redefined diagnostic workup of ATM might include ANE1, as the frequency of this rare disorder might be underestimated.

Factor XIII deficiency as a potential cause of supratentorial haemorrhage after posterior fossa surgery.

BACKGROUND: Postoperative intracranial haemorrhage can be a dramatic event, carrying significant morbidity and mortality. Bleeding at sites remote from the operation area represents a small percentage of haemorrhages whose aetiology remains unclear (Harders et al. Acta Neurochir (Wien) 74(1-2):57-60, 1985). AIM: We present the case of a 60-year-old patient who underwent posterior fossa craniotomy for the removal of a space-occupying lesion and suffered supratentorial haemorrhage soon after the operation. RESULTS: A thorough postoperative investigation revealed low levels of factor XIII (FXIII), the factor mainly responsible for fibrin clot stabilisation. CONCLUSION: We suggest that reduced FXIII activity may be an important but preventable predisposing factor to remote postoperative haemorrhage in neurosurgical patients.

Kinetics of progenitor hemopoetic stem cells in sepsis: correlation with patients survival?

BACKGROUND: Current theories underline the crucial role of pro-inflammatory mediators produced by monocytes for the pathogenesis of sepsis. Since monocytes derive from progenitor hemopoetic cells, the kinetics of stem cells was studied in peripheral blood of patients with sepsis. METHODS: Blood was sampled from 44 patients with septic syndrome due to ventilator-associated pneumonia on days 1, 3, 5 and 7 upon initiation of symptoms. Concentrations of tumour necrosis factor-alpha (TNFalpha), interleukin (IL)-6, IL-8 and G-CSF were estimated by ELISA. CD34/CD45 cells were determined after incubation with anti-CD45 FITC and anti-CD34 PE monocloncal antibodies and flow cytometric analysis. Samples from eight healthy volunteers served as controls. RESULTS: Median of CD34/CD45 absolute count of controls was 1.0/mul. Respective values of the total study population were 123.4, 112.4, 121.5 and 120.9/mul on days 1, 3, 5 and 7 (p < 0.0001 compared to controls). Positive correlations were found between the absolute CD34/CD45 count and the absolute monocyte count on days 1, 5 and 7. Survival was prolonged among patients with less than 310/microl CD34/CD45 cells on day 1 compared to those with more than 310/microl of CD34/CD45 cells (p: 0.022). Hazard ratio for death due to sepsis was 5.47 (p: 0.039) for CD34/CD45 cells more than 310/microl. Median IL-6 on day 1 was 56.78 and 233.85 pg/ml respectively for patients with less than 310/microl and more than 310/microl CD34/CD45 cells (p: 0.021). CONCLUSION: Stem cells are increased in peripheral blood over all days of follow-up compared to healthy volunteers. Patients with counts on day 1 less than 310/microl are accompanied by increased survival compared to patients with more than 310/microl.