Diagnosis and treatment of GBM soft meninges

The results showed that GBM cells migrated from the initial position of the tumor along the soft membrane of cerebrovascular vessels, under the cobweb membrane and under the chamber membrane (Figure 1).
During the migration process, GBM cells can secrete a variety of proteases, such as MMP-1, 2, 7, 9, 14 and 19, where MMP-2 and 9 play a key role in degrading the extracellular substate and expressing a variety of adhesive migration proteins, such as glycosylated sulphate cartilage protein polysaccharides, fibrous proteins, and myoglobin.
synergy between the two molecular cytostebrae, allowing GBM cells to spread and grow along the soft meninges.
Figure 1. A.GBM cell LMS transfer pathway; B. Transfer rate in different spine segments.
two-thirds of LMS occurs within two years of GBM's initial diagnosis.
5 to 16.4 months between initial GBM diagnosis and LMS imaging performance.
tumors that are native to pineal glycoma, spinal cord, around the brain chamber, and in areas of the small brain screen are spaced shorter.
clinical manifestations of LMS can occur from asymptomatic to life-threatening.
of these diseases are craniofacial nerve paralysis, intracranial pressure increase, hydrocephalus formation, false meningitis and refrmpicial neurological dysfunction.
frequency of seizures during the development of LMS was not increased.
rare complications can include sterile high fever, central over-breathing and cardiac arrest.
the GBM tumor can cause stubborn vomiting at an early stage after being sown into the fourth brain chamber.
gliding nerves and facial nerves are the most commonly intruded cranial nerves, and cranial nerve paralysis is often irreversible once it occurs.
of hydrocephaly associated with LMS was not high.
LMS-related factors were age 35-45 years old, where the tumor started, male, long-term survival after initial diagnosis, and tumor volume.
the primary location of tumors is particularly important in the occurrence of LMS, and more LMS occurs under the curtain and in the pineal region of GBM.
that the occurrence of LMS can be assessed from the original location to the brain chamber.
the LMS risk factors that have been agreed upon are the opening of the inoperative brain chamber and multiple operations.
the continued strengthening of the MRI soft meninges after the initial surgery was also associated with a higher rate of LMS.
and molecular characteristics of tumors showed that asstar cell tumors, high expression levels of Ki67/MIB1, and GFAP deficiency were associated with LMS occurrence.
1p36 amplification, PTEN mutation, PlK3CA mutation and MGMT methylation may be potential risk factors for LMS.
for patients with symptoms, enhanced MRI tests found that the sensitivity of LMS in the brain was between 90% and 100%, and that the sensitivity of spinal cord LMS was between 56% and 95%.
it is not clear whether enhanced MRI screening for asymptomatic patients will benefit patients, as LMS performance can be asymptomatic and LMS can occur in patients with stable primary tumor conditions.
LMS is shown on MRI as a line or nod-like lesions, with high signals on MRI-T2 weighted images, low signals on T1 weighted images, and common reinforcement.
MRI characteristic imaging of LMS in the brain had( 1) nodule strengthening, 38% ;(2) soft meninges enhancement, about 47% ;(3) nerve root enhancement, about 57%, and (4) cranial nerve immersion, about 11%-19%.
LMS of the spinal cord, 31% of cases were affected by the neck section of the spinal cord, 52% by the chest, 41% by the waist and 38% by the ponytail and cone.
brain and cerebrospinal fluid analysis suggests that the first positive rate of tumor cells is only 25%-45%.
three consecutive waist wears can increase sensitivity to 86%.
, even when imaging has confirmed LMS, the positive rate of CSF analysis is only 4%-75%.
indirect signs of LMS are elevated intracranial pressure, elevated protein, and sometimes decreased glucose and increased lactic acid.
In recent years, cerebrospinal fluid composition analysis technology has been paid attention to and developed, collecting tumor components floating in cerebrospinal fluid, including circulating tumor cells, ctDNA, RNAs, ctRNA, miRNA and exosomes, etc., which can help the noninvasive diagnosis of CNS tumors and improve the sensitivity of LMS detection.
most cases, LMS in glioma patients is an untreated terminal complication.
has not yet reached a consensus on the treatment of LMS.
, LMS patients had a survival period of 0.2-9.7 months, with an average of 4.7 months.
disease continues to progress or treat related complications, such as intraoperative injections, bleeding or infection after celiac sequestration, can directly lead to the death of the patient.
multi-cooker LMS, surgery cannot be performed.
surgical removal of local nods with severe local nods can relieve symptoms without affecting survival.
up to 20% to 30% of patients with blocky hydrocephaly need VP section.
common complications of cerebrospinal VP striatage include cerebrospinal fluid-high protein-induced striatage valve obstruction, cerebral hemorrhage and meningitis.
rare complications have GBM celiac dispersion.
palliative radiotherapy is the most common treatment for LMS.
radiation doses are usually between 20 and 40gy and can relieve some serious symptoms such as pain.
study showed that isolated trials of radiomark monoclonal antibodies failed to significantly improve survival rates in LMS patients.
more than
clinical trials of chemotherapy drugs commonly used in the use of tymoamine, carmostin, methotrexate, glycosine, etc. for individual or combination of administration, can benefit some patients.
patients can also benefit from drugs such as the anti-angiogenic drug beval monoantigen, alone or in a joint use with the cytotoxic agent Eriticon.
BRAF V600E mutant GBM, mapK pathway inhibitors, BRAF or MEK inhibitors can be used to achieve significant clinical and imaging therapeutic results.
recent studies have shown that IL13R alpha2 targeted chimic antigens (CAR) T-cell therapy LMS has good results.
but the limitations of immunotherapy for GBM, including LMS patients, remain difficult to find suitable targets, immunosuppressive micro-environments, and the toxicity that comes with it.
conclusions The authors conclude that LMS has aggressive behavior and a worse prognosmation in primary malignant central nervous system tumors.
LMS was 4.94 months (2-9 months) after diagnosis.
part of the nodding LMS line surgically removed, its overall survival period can be up to 12 months.
male patients had shorter progressies, but the effect of sex on total survival was not significant.
note that LMS does not seem to have predictive value for lifetime.
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