There are multiple mechanisms by which tumor cells can disseminate into the subarachnoid spaces. Once the tumor cells gain access to the CSF, there is direct communication with the entire subarachnoid space. Tumor cells are carried by bulk flow, with most deposits occurring at the base of the skull or spine.
Tumor cells can hematogenously spread to involve the brain parenchyma or choroid plexus. Once implanted they may rupture seeding the leptomeninges with micrometastases. However, not all patients have concomitant CNS or choroid plexus metastases suggesting that there must be other mechanisms. Detailed pathological review has failed to demonstrate tumor cells within the lumen of the leptomeningeal arterial vasculature; therefore, hematogenous spread through leptomeningeal arteries is unlikely.65 In leukemia, malignant cells enter the subarachnoid space via thin-walled microscopic veins in the arachnoid membrane and seed the meninges.92 Malignant cells also extend into the Virchow-Robin space. Similar mechanisms may also hold true for solid tumors.
Direct extension is a second mechanism by which invasion into the subarachnoid space occurs. This can occur by paravertebral spread along the cranial or spinal nerve roots, invasion of the perineural spaces by the primary focus, cervical lymph nodes communicating directly with the subarachnoid space, and tumor growth into the subdural space. Extension from Batson's plexus and perivenous spread from bone marrow metastases has also been proposed.55 Posterior fossa craniotomies for resection of cerebellar metastases appear to be a risk factor for the development of LM, likely from the proximity of the lesion to the CSF spaces.83,129
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