An elderly patient presenting with a primary spinal multifocal intradural extramedullary pilocytic astrocytoma: a case report and review of the literature.

BACKGROUND: Pilocytic astrocytoma is a low-grade central nervous system tumor most commonly seen in children. Dissemination from a primary intracranial tumor along the neuroaxis has been described at both presentation and disease progression. However, the development of an intradural extramedullary pilocytic astrocytoma independent of a primary intraparenchymal tumor in an adult patient with no history of pilocytic astrocytoma has rarely been reported. CASE PRESENTATION: A 69-year-old woman presented with progressive myelopathic symptoms and thoracic radicular pain. MRI imaging of the whole spine showed an enhancing intradural extramedullary lesion extending from the cervical cord to T11 causing cord compression. Laminectomies were performed for surgical decompression and histopathology was consistent with pilocytic astrocytoma. Complete staging was done that included imaging of the brain and cerebrospinal fluid cytology. No other tumor was found by these methods. Postoperatively the patient was treated with large field spinal radiation and concurrent chemotherapy followed by adjuvant chemotherapy. She has thus far been clinically and radiographically stable. CONCLUSION: This is a rare case of an adult with multiple spinal pilocytic astrocytomas in an intradural extramedullary location, typically the result of cerebrospinal fluid dissemination of neoplastic cells from a primary intracranial tumor site (i.e. drop metastasis). No conventional primary tumor was identified in this patient, suggesting these tumors may arise from heterotopic gliomas.

Global cerebral ischemia due to circulatory arrest: insights into cellular pathophysiology and diagnostic modalities.

Circulatory arrest (CA) remains a major unresolved public health problem in the United States; the annual incidence of which is ~0.50 to 0.55 per 1000 population. Despite seminal advances in therapeutic approaches over the past several decades, brain injury continues to be the leading cause of morbidity and mortality after CA. In brief, CA typically results in global cerebral ischemia leading to delayed neuronal death in the hippocampal pyramidal cells as well as in the cortical layers. The dynamic changes occurring in neurons after CA are still unclear, and predicting these neurological changes in the brain still remains a difficult issue. It is hypothesized that the "no-flow" period produces a cytotoxic cascade of membrane depolarization, Ca2+ ion influx, glutamate release, acidosis, and resultant activation of lipases, nucleases, and proteases. Furthermore, during reperfusion injury, neuronal death occurs due to the generation of free radicals by interfering with the mitochondrial respiratory chain. The efficacy of many pharmacological agents for CA patients has often been disappointing, reflecting our incomplete understanding of this enigmatic disease. The primary obstacles to the development of a neuroprotective therapy in CA include uncertainties with regard to the precise cause(s) of neuronal dysfunction and what to target. In this review, we summarize our knowledge of the pathophysiology as well as specific cellular changes in brain after CA and revisit the most important neurofunctional, neuroimaging techniques, and serum biomarkers as potent predictors of neurologic outcome in CA patients.

Republished: MRI SPACE sequence confirmation of occluded MCA M2 dissection stump masquerading as a ruptured MCA aneurysm.

Intracranial vascular pathologies often have overlapping clinical presentations. Dissected vessel occlusions and bifurcation aneurysms can appear similar on pretherapeutic imaging. The medical management of these two entities is drastically different. The patient is a 51-year-old man who presented with severe, sudden-onset headache. Initial presentation was consistent with a ruptured middle cerebral artery (MCA) aneurysm and surgical clipping was recommended. However, further review of radiographic findings could not definitively differentiate an aneurysmal origin of the symptoms as opposed to intracranial dissection followed by occlusion of the M2 branch of the MCA. MRI sampling perfection with application optimised contrasts using different flip angle evolution (SPACE) was performed and showed thin flow signalling distal to the dissected vessel stump confirming the diagnosis. Accurate diagnosis is a crucial step in directing treatment for intracranial vascular lesions. MRI SPACE is a simple tool in the diagnostic armamentarium to adequately direct treatment and avoid the potential for unnecessary interventions.

MRI SPACE sequence confirmation of occluded MCA M2 dissection stump masquerading as a ruptured MCA aneurysm.

Intracranial vascular pathologies often have overlapping clinical presentations. Dissected vessel occlusions and bifurcation aneurysms can appear similar on pretherapeutic imaging. The medical management of these two entities is drastically different. The patient is a 51-year-old man who presented with severe, sudden-onset headache. Initial presentation was consistent with a ruptured middle cerebral artery (MCA) aneurysm and surgical clipping was recommended. However, further review of radiographic findings could not definitively differentiate an aneurysmal origin of the symptoms as opposed to intracranial dissection followed by occlusion of the M2 branch of the MCA. MRI sampling perfection with application optimised contrasts using different flip angle evolution (SPACE) was performed and showed thin flow signalling distal to the dissected vessel stump confirming the diagnosis. Accurate diagnosis is a crucial step in directing treatment for intracranial vascular lesions. MRI SPACE is a simple tool in the diagnostic armamentarium to adequately direct treatment and avoid the potential for unnecessary interventions.

Endoscopic Endonasal Surgery for the Resection of a Cavernous Hemangioma with a Sellar Extension.

Cavernous hemangiomas with an intrasellar extension are very rare, generally benign lesions that manifest by the compression of nearby structures. The presenting symptoms usually range from visual disturbances to an endocrine imbalance. Occasional extension into the cavernous sinus has been reported, which can cause cranial nerve compression. We present the case of a 69-year-old man presenting with facial pain and decreased libido. On investigation, a lesion was identified and the parasellar region was homogeneously hyper-intense on gadolinium-enhanced magnetic resonance imaging (MRI). Endoscopic endonasal surgery remains one of the favored approaches for the resection of sellar lesions. Such pathology needs to remain on the neurosurgeon's differential diagnosis, making an intraoperative frozen section of these lesions a useful tool in the surgeon's armamentarium, to guide further surgical resection.

Quantitative contrast ratio comparison between T1 (TSE at 1.5T, FLAIR at 3T), magnetization prepared rapid gradient echo and subtraction imaging at 1.5T and 3T.

INTRODUCTION: Creating contrast between normal anatomy and pathology is the main goal of imaging. Here we compare contrast ratios of enhancing brain lesions at 1.5T between T1 TSE, magnetization prepared rapid gradient echo (MPRAGE) and subtraction and at 3T between T1 FLAIR, MPRAGE and subtraction. METHODS: Contrast ratio between enhancing lesions and normal contralateral brain was measured for above mentioned sequences during the same imaging session. A total of 27 exams on 25 patients were evaluated. RESULTS: A total of 90 enhancing brain lesions were utilized. Of these 46 were <5 mm diameter. Taking all lesions into account there was a small but statistically significant improvement in contrast ratio at 1.5T with MPRAGE compared to T1 TSE and at 3T for T1 FLAIR compared to MPRAGE. However, there was no statistically significant difference between these sequences for lesions 5 mm or less in diameter. However, subtraction provided a marked and statistically significant improvement in contrast ratio for both all lesions and including only lesions 5 mm or less in diameter. CONCLUSIONS: Our data indicate that for small lesions at 1.5T there is no significant difference in contrast ratio (CR) between T1 TSE and MPRAGE or at 3T between T1 FLAIR and MPRAGE despite the MPRAGE having the advantage of much thinner slices and a higher matrix. However, subtraction provided a markedly improved CR for all lesions at 1.5T and 3T regardless of lesion size. Subtraction should be considered for clinical use to improve detection of small or subtle enhancing lesions.