BackgroundPatients with intravascular lymphoma (IVL) frequently have neurological signs and symptoms. Prompt diagnosis and treatment is therefore crucial for their survival. However, the spectrum of neurological presentations and their respective frequencies have not been adequately characterized. Our aim is to document the spectrum of clinical symptoms and their respective frequencies and to create a clinical framework for the prompt diagnosis of IVL.MethodsA comprehensive meta-analysis of 654 cases of IVL published between 1957 and 2012 was performed to provide better insight into the neurological presentations of this disease. Neurologic complications were mainly divided into central nervous system (CNS) and peripheral nervous system (PNS) presentations.ResultsThere were no differences in occurrences of CNS IVL based on gender or geographic locations (Asian Vs non-Asian). However, most patients with CNS IVL were younger than 70 years of age (p < 0.05). Our limited data do not support the treatment efficacy of methotrexate.CNS symptoms were seen in 42 % of all cases. The most common CNS complications identified were cognitive impairment/dementia (60.9 %), paralysis (22.2 %), and seizures (13.4 %). PNS complications were seen in 9.5 % of cases. Out of these, muscle weakness (59.7 %), neurogenic bladder (37.1 %), and paresthesia (16.1 %) were the most common presentations.ConclusionsCNS complications are more common among IVL patients. Out of these, dementia and seizures outnumber stroke-like presentations.Electronic supplementary materialThe online version of this article (doi:10.1186/s12883-015-0509-8) contains supplementary material, which is available to authorized users.
Annually, there are over 2 million incidents of traumatic brain injury (TBI) and treatment options are non-existent. While many TBI studies have focused on the brain, peripheral contributions involving the digestive and immune systems are emerging as factors involved in the various symptomology associated with TBI. We hypothesized that TBI would alter hepatic function, including bile acid system machinery in the liver and brain. The results show activation of the hepatic acute phase response by 2 hours after TBI, hepatic inflammation by 6 hours after TBI and a decrease in hepatic transcription factors, Gli 1, Gli 2, Gli 3 at 2 and 24 hrs after TBI. Bile acid receptors and transporters were decreased as early as 2 hrs after TBI until at least 24 hrs after TBI. Quantification of bile acid transporter, ASBT-expressing neurons in the hypothalamus, revealed a significant decrease following TBI. These results are the first to show such changes following a TBI, and are compatible with previous studies of the bile acid system in stroke models. The data support the emerging idea of a systemic influence to neurological disorders and point to the need for future studies to better define specific mechanisms of action.
Levetiracetam, trade name Keppra, is a new second generation antiepileptic drug that is being increasingly used in brain tumor patients. In patients suffering with brain tumors, seizures are one of the leading neurologic complications being seen in more than 30% of patients. Unlike other antiepileptic drugs, levetiracetam is proposed to bind to a synaptic vesicle protein inhibiting calcium release. Brain tumor patients are frequently on chemotherapy or other drugs that induce cytochrome P450, causing significant drug interactions. However, levetiracetam does not induce the P450 system and does not exhibit any relevant drug interactions. Intravenous delivery is as bioavailable as the oral medication allowing it to be used in emergency situations. Levetiracetam is an attractive option for brain tumor patients suffering from seizures, but also can be used prophylactically in patients with brain tumors, or patients undergoing neurological surgery. Emerging studies have also demonstrated that levetiracetam can increase the sensitivity of Glioblastoma tumors to the chemotherapy drug temozolomide. Levetiracetam is a safe alternative to conventional antiepileptic drugs and an emerging tool for brain tumor patients combating seizures.
More patients are now being diagnosed with nonpalpable prostate cancer after a needle biopsy is performed for an elevated prostate-specific antigen (PSA) level (stage T1c). The purpose of this study was to identify prognostic factors that are associated with biochemical failure after definitive external beam radiation therapy. This study included 75 patients with the diagnosis of T1c prostate cancer who were referred to four radiation oncology centers in the West Chicago area from 1992 to 1995. All patients were treated with megavoltage external beam radiotherapy to doses between 66 and 70 Gy. Biochemical failure was defined as three consecutive rising PSA values of at least 10% of the prior reading in posttreatment serial measurements. The mean age of the patients was 72 years. The mean follow-up was 1.7 years (range, 1-3 1/2 years). Of the 75 patients, 72 (96%) are clinically with no evidence of disease, three of the 75 are alive with disease, and 60 (80%) remain biochemically free of disease (bNED). The significant factors for bNED status were an initial PSA level of <15 ng/ml (p = 0.0001), achievement of a posttreatment nadir PSA level of < or = 1.5 ng/ml (p = 0.0001), and a Gleason score of <6 (p = 0.034). Multisextant involvement with tumor or bilobar disease was not significant. On multivariate analysis, an initial PSA level of <15 ng/ml (p = 0.0001), Gleason score of <6 (p = 0.02), and nadir PSA level of < or = 1.5 ng/ml (p = 0.03) were significant predictors of bNED survival. Men with T1c prostate cancer comprise a heterogeneous group. Patients with a high PSA level (>15 ng/ml) and high Gleason score (>6) are at increased risk for biochemical failure. Failure to achieve a posttreatment nadir PSA level of < or = 1.5 ng/ml is a predictor of ultimate biochemical failure.
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