Congenital glioblastoma multiforme: case report and review of the literature.

Congenital glioblastoma multiforme is a rare primary brain tumor that has a unique biology distinct from pediatric and adult variants. In this report, we present a case of congenital glioblastoma with complicated management course. A literature review of previously reported cases is included to illustrate the epidemiology and natural history of this disease. A 9-month-old male infant developed acute lethargy, hemiparesis and unilaterally dilated pupil. Imaging studies revealed a large hemispheric tumor, resulting in significant midline shift suggestive of impending herniation. Emergent tumor cystic fluid drainage was performed at initial presentation. A frontotemporoparietal craniotomy was performed on the following day to attempt a gross total resection. Adjuvant chemotherapy consisting of oral temozolomide was administered. The patient eventually succumbed 4 months later due to aggressive tumor progression. Congenital glioblastoma should be included in the differential diagnosis of infants with large intracranial tumors. Although surgical intervention may increase survival, the overall outcome remains poor despite maximal multimodal treatment.

Molecular events of brain metastasis.

The brain is a privileged site of systemic cancer metastasis. The stages of the metastatic journey from the periphery to the brain are driven by molecular events that tie the original site of disease to the distant host tissue. This preference is not arbitrary but rather a directed phenomenon that includes such critical steps as angiogenesis and the preparation of the premetastatic niche. It appears that the connection between naive brain and cancer cells is made in advance of any metastatic breach of the blood-brain barrier. This contributes to the preferential homing of cancer cells to the brain. Delineation of the guidance mechanisms and elements that influence cancer cell motility and dormancy are important for the advancement of treatment modalities aimed at the remediation of this devastating disease.

High-LET radiation induces inflammation and persistent changes in markers of hippocampal neurogenesis.

Exposure to heavy-ion radiation is considered a potential health risk in long-term space travel. It may result in the loss of critical cellular components in complex systems like the central nervous system (CNS), which could lead to performance decrements that ultimately could compromise mission goals and long-term quality of life. Specific hippocampal-dependent cognitive impairment occurs after whole-body 56Fe-particle irradiation, and while the pathogenesis of this effect is not yet clear, it may involve damage to neural precursor cells in the hippocampal dentate gyrus. We irradiated mice with 1-3 Gy of 12C or 56Fe ions and 9 months later quantified proliferating cells and immature neurons in the dentate subgranular zone (SGZ). Our results showed that reductions in these cells were dependent on the dose and LET. When compared with data for mice that were studied 3 months after 56Fe-particle irradiation, our current data suggest that these changes are not only persistent but may worsen with time. Loss of precursor cells was also associated with altered neurogenesis and a robust inflammatory response. These results indicate that high-LET radiation has a significant and long-lasting effect on the neurogenic population in the hippocampus that involves cell loss and changes in the microenvironment.

Spontaneous intracranial hypotension associated with transdural thoracic osteophyte reversed by primary. dural repair. Case report.

Spontaneous intracranial hypotension (SIH) is an increasingly recognized syndrome associated with a specific set of clinical and imaging findings; however, determining the site of spinal cerebrospinal fluid (CSF) leakage in these patients is often difficult, and indications for surgical intervention need to be better defined. The authors report on a 55-year-old woman who presented with posture-related headache, disorientation, and memory impairment. Imaging features were consistent with SIH. Computerized tomography myelography demonstrated a large T2-3 anterior transdural osteophyte associated with a CSF fistula. After an unsuccessful trial of conservative therapy, the patient underwent median sternotomy, T2-3 discectomy and removal of osteophyte, which allowed adequate exposure for primary dural repair. Postoperatively, there was immediate and prolonged resolution of all of her symptoms. This case of SIH was caused by transdural penetration by an anterior osteophyte and CSF leakage in the upper thoracic spine, which was treated effectively by anterior exposure and primary dural repair. Aggressive surgical intervention may be required to treat upper thoracic CSF leaks refractory to other measures.

The sequelae of cranial irradiation on human cognition.

Cranial irradiation (CI) confers remediation of many CNS anomalies. CI, however, carries risks to cognitive performance. A wealth of data describes such deficits specifically in humans. Risk factors that promote increased susceptibility to cognitive decline have also been identified. This paper discusses and grades these risk factors, including age, gender, and the inclusion of chemotherapy, that increase the likelihood of pathologic cognitive development in the human population.

Resolution of intracranial hypertension after elevation of depressed cranial fracture over the superior sagittal sinus: case report.

OBJECTIVE AND IMPORTANCE: It is common neurosurgical wisdom that depressed cranial fractures (DCFs) over the superior sagittal sinus (SSS) should not be elevated because of the risk of fatal venous hemorrhage. CLINICAL PRESENTATION: A 34-year-old man presented with severe headache and diplopia after a motor vehicle accident. Clinical examination demonstrated severe papilledema and bilateral abducens palsy. Imaging findings demonstrated a DCF over the posterior third of the SSS and absent flow distal to the fracture with dilated cortical venous drainage. INTERVENTION: Conservative treatment with acetazolamide only partially alleviated the patient's headache and diplopia. Definitive surgical treatment via elevation of the DCF was discussed and decided upon. Twelve days after injury, the patient underwent midline parieto-occipital craniotomy with successful elevation of the DCF off the posterior third of the SSS. Postoperative magnetic resonance venograms revealed restoration of patency in the SSS with reduced tortuosity of cortical veins. The patient's headache resolved, and his papilledema and diplopia resolved gradually. CONCLUSION: Elevation of DCF over the SSS can be attempted in cases in which favorable bone anatomy and the patient's clinical condition warrant. This may result in rapid and dramatic resolution of signs and symptoms of secondary intracranial hypertension.