Leptomeningeal disease: current diagnostic and therapeutic strategies

Abstract

Leptomeningeal disease has become increasingly prevalent as novel therapeutic interventions extend the survival of cancer patients. Although a majority of leptomeningeal spread occurs secondary to breast cancer, lung cancer, and melanoma, a wide variety of malignancies have been reported as primary sources. Symptoms on presentation are equally diverse, often involving a combination of neurological deficits with the possibility of obstructive hydrocephalus. Diagnosis is definitively made via cerebrospinal fluid cytology for malignant cells, but neuro-imaging with high quality T1-weighted magnetic resonance imaging can aid diagnosis and localization. While leptomeningeal disease is still a terminal, late-stage complication, a variety of treatment modalities, such as intrathecal chemotherapeutics and radiation therapy, have improved median survival from 4–6 weeks to 3–6 months. Positive prognosticative factors for survival include younger age, high performance scores, and controlled systemic disease. In looking to the future, diagnostics that improve early detection and chemotherapeutics tailored to the primary malignancy will likely be the most significant advances in improving survival.

Pan-Asian adapted Clinical Practice Guidelines for the management of patients with metastatic non-small-cell lung cancer: a CSCO–ESMO initiative endorsed by JSMO, KSMO, MOS, SSO and TOS

“…LMD is a deadly complication of solid tumours and is associated with a poor prognosis. Of the patients with NSCLC who present with CNS metastases (30%-64%), 4%-7% present with LMD [252]. The incidence and prevalence of LMD is increasing due to screening for brain metastases, better imaging modalities, as well as a prolongation of patient survival in those with CNS metastases.…”

Papilledema and Bilateral Optic Neuropathy: Dual Mechanism for Visual Loss in a Patient with Leptomeningeal Carcinomatosis

“…There are several proposed mechanisms for increased intracranial pressure in patients with LC: it may be secondary to high levels of CSF protein due to leptomeningeal seeding by cancer cells which increases CSF viscosity and leads to its decreased outflow. Another possibility is cerebral edema secondary to increased cerebral vascular endothelial permeability due to aberrant stimulation of the meninges by tumor cells causing release of various chemical mediators 6 . Lastly, tumor cells may directly block arachnoid granulations, the presumed main site of CSF absorption.…”

Ommaya Reservoir Related Complications: A Single Center Experience and Review of Current Literature

“…Tables 2 and 3 show OmR specific data for all 13 patients, along with their expected survival. [13][14][15][16][17][18][19] Infectious and noninfectious complications are shown in Figure 2.…”