Pleomorphic xanthoastrocytoma (PXA) is a rare primary CNS tumor. Recent advances in the molecular characterization are helping to define subtypes of tumor. The discovery of BRAF mutations within a substantial percentage of PXA fosters a clearer understanding of the pathophysiology of these tumors with clear prognostic and therapeutic implications. These findings are expected to provide insight into the spectrum of clinical behavior observed in PXA, ranging from cure with surgery to diffuse dissemination throughout the neuraxis. This review details the clinical presentation including radiographic appearance of PXA. Pathology, including molecular pathology is discussed. Therapeutic management including surgical resection, radiotherapy and systemic therapies are reviewed.

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Cervical lymphadenopathy is a common condition characterized by the enlargement of lymph nodes. It can have various causes, including infections, inflammatory conditions, and neoplastic processes. Syphilis, a sexually transmitted disease that progresses through multiple stages, can also be a rare cause of cervical lymphadenopathy, particularly in HIV-positive individuals. In this case report, we describe a patient presenting with throat pain, systemic symptoms, and cervical lymphadenopathy, initially clinically suggestive of lymphoma but ultimately determined to be caused by syphilis of unknown duration. This case highlights the importance of considering syphilis in the differential diagnosis of cervical lymphadenitis, particularly in patients with risk factors, such as intravenous drug use and HIV infection, and the need for a thorough evaluation of the patient's social and medical histories to diagnose and treat the condition accurately.

A 22-year-old right-handed man with recently diagnosed gout and renal insufficiency presented with three months of progressive gait instability and cognitive changes. He initially presented to an outside institution and underwent a broad workup, but an etiology for his symptoms was not found. On subsequent presentation to our institution, his exam revealed multi-domain cognitive dysfunction, spasticity, hyperreflexia and clonus. A broad workup was again pursued and was notable for an MRI of the brain revealing cortical atrophy advanced for his age, bland cerebrospinal fluid, and a weakly positive serum acetylcholine receptor ganglionic neuronal antibody of unclear significance. The history of gout and inadequately explained renal insufficiency led to a workup for inborn errors of metabolism, including urine amino acid analysis, which revealed a homocysteine peak. This finding prompted further evaluation, revealing markedly elevated serum homocysteine and methylmalonic acid and low methionine. He ultimately developed superficial venous thromboses and a segmental pulmonary embolism, as well as clinical and electrographic seizures. He was initiated on appropriate treatment, and his symptoms markedly improved. The case serves as a reminder to include late-onset inborn errors of metabolism in the differential for young adult patients with onset of neurological, psychiatric, renal, and thromboembolic symptoms.