Glioblastoma (GBM) is a highly aggressive primary tumor in adults, composing of 12-20% of intracranial tumors and more than 50% of glial neoplasms, it is classified as a Grade 4 tumor according to the World Health Organization (WHO) classification of brain tumors [6].

Glioblastoma (GBM) was first described by Rudolph Virchow in 1863 [1], and represents the most common and most malignant tumor of the cerebral hemispheres, typically occurring between the ages of 40 and 60 years. The incidence in Europe and North America is estimated at 2 to 3 cases per 100,000 individuals per year, with 75% of patients succumbing to the disease within 18 months following diagnosis.

The incidence of spinal metastasis of cerebral glioblastoma is approximately 1.1% in the published literature. [7], in a serial autopsy study, approximately 25% of patients with intracranial GBM demonstrated spinal subarachnoid seeding; however, the exact incidence remains unknown [8].

The incidence of GBM metastasizing to the spinal compartment is likely higher than what is clinically detected, suggesting that spinal metastases have been underestimated in current clinical practice [9].

It is an infiltrating malignancy that recurs locally and it may spread along compact fiber pathways such as corpus callosum, optic irradiation, anterior commisure, and fornix or via cerebrospinal fluid (CSF) pathways. [10-11], cerebrospinal seeding (CSF) is present in approximately 15-25% of the cases of supratentorial GBM, while a higher incidence is seen in patients with infratentorial GBM [12].

When tumor cells infiltrate the Cerebrospinal Fluid (CSF) pathways, they can disseminate to any structure in direct contact with CSF, including the peritoneal cavity in cases where a ventriculoperitoneal shunt (VPS) is implanted.

The risk of spinal dissemination of tumor cells is increased following craniotomy, intraoperative ventricular entry, multiple resections, and in male patients [13]. Additional risk factors for CSF dissemination include ependymal invasion, ependymal fissuring due to hydrocephalus, and fragmentation of the tumor in contact with CSF.

Repeated tumor resection is associated with an increased risk of CSF dissemination, because of repeated tumor manipulation, more aggressive tumor cell types, and depressed immune function after radiotherapy and chemotherapy [14,15].

In a study on supratentorial gliomas in children conducted by Grabb et al., these factors were all found to be statistically significant contributors to the increased incidence of CSF dissemination [16].

The most frequent sites of spinal GBM metastases are the lower thoracic, upper lumbar, and lumbosacral regions. Spinal metastases commonly involve the nerve roots of the cauda equina, the root sleeves, and the fundus of the thecal sac, intramedullary metastases are exceedingly rare, with only a few cases reported in the literature [17].

Common symptoms of spinal metastasis include radicular pain, sensory loss, gait disturbances, and weakness. Patients may also experience pain in the lower back, interscapular area, and neck. As the condition progresses, paraparesis, quadriparesis, paraplegia, bowel or bladder dysfunction, and sexual dysfunction may develop [18]

Spinal MRI with gadolinium enhancement is currently the investigation of choice for diagnosing spinal metastasis. Lumbar CSF cytology is not routinely employed for this purpose due to the high incidence of false negative results.

The detection of tumor cells in the CSF is considered the most reliable criterion for diagnosing metastatic spinal dissemination (MSD) in GBM; but the chances of positive cytology are low. In a study by Chen et al., CSF cytology was found to be negative in all 14 observed cases [19].

Thus, whole spinal cord-enhanced MRI is currently considered the most effective diagnostic tool for metastatic spinal dissemination (MSD) in clinical practice.

There are no established guidelines for treatment of spinal metastasis from cerebral glioblastoma.

After the diagnosis of spinal metastasis, chemoradiotherapy is the primary treatment approach. Surgery may be considered for focal lesions, but chemoradiotherapy remains the only viable option for patients with diffuse or leptomeningeal disease.

The Stupp protocol, administered after initial brain surgery, does not appear to offer any survival benefit for patients with spinal metastases. The primary treatment goal is to alleviate pain and neurological deficits, without significantly impacting overall survival [1].

Unfortunately, the prognosis is very poor, with fatal outcomes. The time interval between the diagnosis of metastases and death ranges from 2 to 20 months, with an average survival of 2 to 3 months. Younger individuals tend to have a somewhat better prognosis [20-21].