NEUROLOGIC MANIFESTATIONS OF LEUKEMIA

PEDIATRICS ◽  
1957 ◽  
Vol 19 (5) ◽  
pp. 801-809
Author(s):  
Enid F. Gilbert ◽  
E. Clarence Rice

Three cases of acute lymphocytic leukemia with neurologic manifestations are presented in which the clinical signs, together with the findings in the spinal fluid, closely resembled those of acute bacterial meningitis. Review of the literature reveals an infrequent occurrence of neurologic symptoms in leukemia. When present, they usually represent a terminal phenomenon. The occurrence of a low content of sugar in the cerebrospinal fluid in association with meningeal infiltration of the brain in patients with leukemia has been reported. The relation of this phenomenon to the glycolytic activity of leukemic cells is discussed.

Blood ◽  
1980 ◽  
Vol 55 (4) ◽  
pp. 702-705
Author(s):  
ER Richie ◽  
MP Sullivan ◽  
J van Eys

A 5-yr-old girl with acute lymphocytic leukemia presented with moderate hepatomegaly, marked splenomegaly, but no evidence of a mediastinal mass. The peripheral blood white count was 270 x 10(9)/liter with 99% leukemic cells. Surface marker analysis showed the lymphoblasts to be E- rosette negative and complement receptor positive. The patient's leukemic cells were unreactive with anti-p23,30, which detects Ia-like antigens, and strongly reactive with A99 anti-T-cell serum, which reacts with normal human thymocytes and peripheral blood T cells. The percentage of leukemic cells bearing complement receptors diminished during relapse. The leukemic cells obtained at diagnosis and during relapse were nonreactive to mitogens and alloantigens and failed to stimulate proliferation of normal lymphocytes in mixed lymphocyte culture. There was no evidence for active suppression of normal lymphocyte reactivity mediated by the leukemic cells. The surface marker and functional profile of these leukemic cells is consistent with that of an early stage in T-cell maturation.


Blood ◽  
1990 ◽  
Vol 76 (2) ◽  
pp. 285-289 ◽  
Author(s):  
TC Meeker ◽  
D Hardy ◽  
C Willman ◽  
T Hogan ◽  
J Abrams

Abstract The t(5;14)(q31;q32) translocation from B-lineage acute lymphocytic leukemia with eosinophilia has been cloned from two leukemia samples. In both cases, this translocation joined the IgH gene and the interleukin-3 (IL-3) gene. In one patient, excess IL-3 mRNA was produced by the leukemic cells. In the second patient, serum IL-3 levels were measured and shown to correlate with disease activity. There was no evidence of excess granulocyte/macrophage colony stimulating factor (GM-CSF) or IL-5 expression. Our data support the formulation that this subtype of leukemia may arise in part because of a chromosome translocation that activates the IL-3 gene, resulting in autocrine and paracrine growth effects.


Blood ◽  
1992 ◽  
Vol 79 (8) ◽  
pp. 2076-2083 ◽  
Author(s):  
D Grander ◽  
M Heyman ◽  
K Brondum-Nielsen ◽  
Y Liu ◽  
E Lundgren ◽  
...  

Abstract Various aspects of the interferon (IFN) system were studied in malignant cells from 37 unselected patients with acute lymphocytic leukemia (ALL). It was found that leukemic cells from two of 37 patients had a complete loss of alpha- and beta-IFN genes, whereas cells from four of 37 had lost one of the alpha-/beta-IFN alleles. In 25 cases, viable cells were also available for functional studies. Cell clones with loss of one of the alpha-/beta-IFN alleles produced low amounts of IFN after virus induction in vitro. Some clones with an apparently normal set of IFN genes were unable to produce detectable amounts of IFN. All clones studied were found to carry high-affinity alpha-IFN receptors. In clones carrying deletions of IFN genes, the cells were sensitive to IFN in vitro as measured by alpha-IFN-induced enhancement of 2′,5′-oligoadenylate synthetase (2′,5′-A synthetase). Cells from four patients with an apparently normal set of IFN genes were insensitive to this effect of IFN. We conclude that of the 17 patients in which IFN genes, IFN production, alpha-IFN receptors, and IFN-induced enhancement of 2′,5′-A synthetase were studied, nine (53%) showed some abnormality in their IFN system. This finding may add some support to the hypothesis that defects in the IFN system could be a step on the path to malignant transformation in ALL. Moreover, patients whose malignant cells carry IFN gene deletions or other defects in their IFN-producing capacity, but are still sensitive to exogenous IFN, could represent a subgroup of ALL with a greater likelihood of responding to IFN therapy.


2006 ◽  
Vol 104 (5) ◽  
pp. 810-819 ◽  
Author(s):  
Mark E. Wagshul ◽  
John J. Chen ◽  
Michael R. Egnor ◽  
Erin J. McCormack ◽  
Patricia E. Roche

Object A recently developed model of communicating hydrocephalus suggests that ventricular dilation may be related to the redistribution of pulsations in the cranium from the subarachnoid spaces (SASs) into the ventricles. Based on this model, the authors have developed a method for analyzing flow pulsatility in the brain by using the ratio of aqueductal to cervical subarachnoid stroke volume and the phase of cerebrospinal fluid (CSF) flow, which is obtained at multiple locations throughout the cranium, relative to the phase of arterial flow. Methods Flow data were collected in a group of 15 healthy volunteers by using a series of images acquired with cardiac-gated, phase-contrast magnetic resonance imaging. The stroke volume ratio was 5.1 ± 1.8% (mean ± standard deviation). The phase lag in the aqueduct was −52.5 ± 16.5° and the phase lag in the prepontine cistern was −22.1 ± 8.2°. The flow phase at the level of C-2 was +5.1 ± 10.5°, which was consistent with flow synchronous with the arterial pulse. The subarachnoid phase lag ventral to the pons was shown to decrease progressively to zero at the craniocervical junction. Flow in the posterior cervical SAS preceded the anterior space flow. Conclusions Under normal conditions, pulsatile ventricular CSF flow is a small fraction of the net pulsatile CSF flow in the cranium. A thorough review of the literature supports the view that modified intracranial compliance can lead to redistribution of pulsations and increased intraventricular pulsations. The phase of CSF flow may also reflect the local and global compliance of the brain.


Blood ◽  
1981 ◽  
Vol 57 (5) ◽  
pp. 879-882 ◽  
Author(s):  
E Morgan ◽  
CC Hsu

Abstract Peripheral blood samples from 57 children with newly diagnosed E- rosette-negative, surface-immunoglobulin negative acute lymphocytic leukemia (ALL) were studied for the presence of a leukemia-associated antigen (ALLA). Ficoll-Hypaque separated cells were tested using a rabbit antiserum to human null lymphoblasts and an indirect immunofluorescent assay. The percentage of ALLA-positive cells were compared to the percentage of lymphoblasts determined by differential counts of a Wright-Giemsa-stained smear of a concurrently obtained peripheral blood sample. The mean ratio of percentage of lymphoblasts to percentage of ALLA-positive cells was 0.90. However, in 13 patients, the ratio of percent of ALLA-positive cells to percent of lymphoblasts was equal to or greater than 2:1. In the blood of 6 additional children (5 newly diagnosed, 1 relapsed patient) in whom no morphologically identifiable lymphoblasts were detected. ALLA-positive cells were present (7%-49%). These results indicate that testing for ALLA-positive cells in a sensitive technique for detection of leukemic cells in children with ALLA-positive ALL.


2012 ◽  
Vol 10 (5) ◽  
pp. 457-458
Author(s):  
Paul E. Kaloostian ◽  
Han Chen ◽  
Frederick Rupp ◽  
Erich Marchand

The authors report the case of a 16-year-old boy with pre-B cell acute lymphocytic leukemia diagnosed 2 weeks earlier. On workup for diffuse headaches he was found to have 10-mm bilateral subdural hygromas with compression of the underlying gyri. He was followed clinically, and 4 days after his initial presentation he underwent MRI studies of the brain, which showed complete resolution of the subdural fluid collections. No change in management was noted during these 4 days. This case is the first known instance of rapid, spontaneously disappearing bilateral subdural hygromas in a pediatric patient.


2015 ◽  
Vol 11 (2) ◽  
pp. 1143-1145 ◽  
Author(s):  
DANYI XU ◽  
GUANHUA XU ◽  
LIQIN XU ◽  
HENG CAO ◽  
BEI XU ◽  
...  

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