Abstract. Reversible posterior leukoencephalopathy syndrome (RPLS) is a rare neurological syndrome of the brain, causing symptoms such as headaches, seizures, altered mental status and visual disturbances. The condition is predominantly associated with hypertension, eclampsia, renal impairment, cytotoxic drugs, immunosuppressive agents and molecular targeted agents, but the precise underlying mechanism of RPLS is not fully understood. The present study describes the case of a 65-year-old female patient with stage IIA non-small cell lung cancer who received cisplatin/pemetrexed treatment at the Leo W. Jenkins Cancer Center. Following 3 cycles of this therapy, the patient was referred to the Emergency Department of Vidant Medical Center with an altered mental status, subsequently presenting with epileptic seizures, a fever and a headache. A neurological examination revealed generalized hyperreflexia and paraparesis, with extensor posturing of the bilateral lower extremities. The lumbar puncture and electroencephalography results were normal, but cranial computed tomography (CT) scans revealed attenuation abnormalities in the bilateral parietal region and the left occipital lobe, with suspected metastasis. Cranial T2-weighted magnetic resonance imaging (MRI) indicated bilateral regions of increased signal intensity in the occipital, temporal and periventricular white matter. The patient was treated with anticonvulsants, steroids and antihypertensive drugs, recovered gradually from the symptoms and regained full consciousness. However, the patient reported residual weakness, presenting with an Eastern Cooperative Oncology Group score of 3, reflective of an inability to independently perform daily activities and self-care. A brain MRI performed 10 days later demonstrated that the subcortical edema had partially subsided. The patient was discharged on day 15 post-admission. A follow-up cranial CT examination 1 month later indicated a partial resolution of the abnormalities. The present report reviews similar associated cases, and also discusses the clinical features and mechanisms underlying RPLS. Although it is typically reversible, RPLS is a serious and potentially life-threatening adverse condition if left untreated. Early recognition of this condition is crucial for the prompt control of the patient's blood pressure or withdrawal of cytotoxic drugs in order to reverse this syndrome. IntroductionReversible posterior leukoencephalopathy syndrome (RPLS) was first described by Hinchey et al (1) as an acute illness that causes symptoms such as hypertension, headaches, seizures, altered mental status and visual disturbances, and which is usually reversible following the removal of the causative agents and the control of the patient's blood pressure. RPLS is characterized by white matter edema, particularly involving the bilateral occipital and posterior parietal lobes of the brain (1). Involvement of other areas of the brain, including the frontal lobes, cerebellum, basal ganglia and brain stem, has also been reported.R...
AimsCardiovascular dysautonomia may impact the quality of life and survival in amyotrophic lateral sclerosis (ALS). Such dysfunction is not systematically assessed in these patients. Wearable devices could help. The feasibility of a wearable biosensor to detect heart rate variability (HRV), a physiological marker of sympathovagal balance, was studied for the first time in real-world settings in ALS.MethodsFive ALS patients (two early/three late; one bulbar-onset; mildly-to-moderately disabled) and five age/sex/BMI/comorbidities-matched controls underwent assessment of 3-day HRV via VitalConnect biosensor (worn on the left thorax). De-identified data captured by the biosensor were transferred to a secure cloud server via a relay Bluetooth device. Baseline ALS severity/anxiety and physical activity during testing were documented/quantified. Time-domain HRV measures (i.e., pNN50) were analyzed.ResultsAn overall 3-day abnormal HRV (pNN50 < 3%), was found in three out of five patients (mean ± SD for the group, 2.49 ± 1.51). Similar changes were reported in controls (12.32 ± 21.14%). There were no statistically significant relationships between pNN50 values and baseline anxiety or physical activity during the tested days (p > 0.05 for both groups). A negative correlation was found between pNN50 values and age in patients (p = 0.01) and controls (p = 0.09), which is similar with what is found in the general population. In line with prior studies, pNN50 values were independent of disease stage (p = 0.6) and disability (p = 0.4).ConclusionsThese preliminary results suggest that remote HRV measures using the VitalConnect is feasible and may constitute an improved strategy to provide insights into sympathovagal balance in ALS. Further work with larger sample sizes is warranted.
Multicellular organisms depend on cell‐cell interactions to coordinate their development. In C. elegans, germline stem cell fate depends on the activity of the Notch receptor homolog, glp‐1. The loss of glp‐1 function prevents germ cell proliferation and produces sterile hermaphrodites. To identify new genes that regulate germline proliferation, suppressors of the temperature sensitive allele glp‐1(q231) have been isolated. These mutants, sog (suppressor of glp‐1), rescue sterility of q231 at 20°C. The sog‐1 gene was previously mapped to a 2 Mbp region on chrI. To [LL1]identify the gene responsible for the sog‐1 phenotype, we used Solexa sequencing to re‐sequence the entire genome of two independently isolated sog‐1 mutants. In the critical region, we identified 62 SNPs between the two strains and the reference genome. We performed RNAi screens of candidate genes to test whether they phenocopy sog‐1 suppression of glp‐1. RNAi screens of pbrm‐1 displayed an embryonic lethal phenotype for all strains, while unc‐14 and F57B10.3 potentially phenocopy the germline suppression of q231 by sog‐1. [LL2]Screens of other potential candidates were negative. These results may help identify new genes in germline proliferation and determine if Solexa sequencing will be useful in identifying genes defined by mutation.This work was funded by NIH/HIGMS MARC U*STAR T34 08663 National Research Service Award to UMBC, HHMI and BioMedRAP.
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