Multiple myeloma (MM) is an incurable clonal B-cell malignancy that usually presents with neoplastic monoclonal plasma cells in either bone or soft tissues. Central nervous system involvement of the myeloma (CNS-MM), such as dural myeloma or intraparenchymal infiltration, or diffuse leptomeningeal involvement, is uncommon. Dural involvement of myeloma without parenchymal or leptomeningeal disease is even rarer, with only seven cases reported previously.We present a case of epidural myeloma in a 50-year-old man with known kappa light chain MM, presenting with multiple episodes of subdural hemorrhage and progressive neurological deficits. He initially presented with severe back pain, hypercalcemia, and acute kidney injury (AKI). Further evaluation showed lytic bone lesions and elevated kappa light chains, and bone marrow biopsy showed 32% of clonal plasma cells. He was initially treated with bortezomib, lenalidomide, and dexamethasone combination, followed by pomalidomide and daratumumab. Eventually, he developed two episodes of subdural hemorrhage and leftsided seventh cranial nerve palsy, which was treated conservatively and monitored by computed tomography (CT) of the head. However, he gradually developed multiple cranial nerve palsies, weakness, and urinary incontinence. Cerebrospinal fluid (CSF) analysis showed elevated protein without any aberrant immunophenotype. Magnetic resonance imaging (MRI) of the brain showed diffuse smooth dural enhancement with extensive calvarial and skull base marrow replacement; MRI of the spine showed diffuse epidural enhancement in thoracic and lumbar regions, findings consistent with epidural myeloma. The patient received three doses of cranial irradiation but, unfortunately, could not tolerate further treatment and opted for hospice care.Intracranial hemorrhage is common in MM patients, and it is important to consider CNS involvement in patients presenting with recurrent subdural hemorrhage and to perform imaging (preferably MRI) earlier in the disease course. Due to its rarity, the treatment of CNS-MM is very heterogeneous. Thus, case reporting is important to accumulate data on this rare presentation.

Posterior reversible encephalopathy syndrome (PRES) is a reversible neurological syndrome characterized by headache, seizures, altered mental status, and visual abnormalities, in association with the characteristic bilateral white matter abnormalities in the posterior cerebral hemispheres. As the name suggests, it is typically reversible with clinical recovery within a few days, while the magnetic resonance imaging (MRI) abnormalities resolve much more slowly. We present a 78-year-old female with a known diagnosis of primary myelofibrosis (PMF), on ruxolitinib, a Janus kinase (JAK) 1 and 2 inhibitor, presenting with altered mental status. On presentation, she was hypertensive and with possible sepsis, secondary to urinary tract infection (UTI). She was intubated because of her low Glasgow Coma Scale (GCS), to secure her airways. Computed tomography (CT) of the brain did not reveal any acute ischemic changes. MRI of the brain exhibited findings suggestive of PRES. Ruxolitinib was held and the patient was treated with antihypertensives, anticonvulsants, and antibiotics. Within 24 hours of hospitalization, the patient had a complete neurological recovery, which is diagnostic of PRES. She was extubated successfully and was discharged with a resolution of her symptoms. Although several chemotherapeutic and immunosuppressant drugs are reported to be associated with PRES, the association between ruxolitinib and PRES has not been well established. Thus, case reporting is important to highlight the possible association between ruxolitinib and PRES.

Sudden blast crisis is an uncommon phenomenon in chronic myeloid leukemia (CML) patients who are being treated with tyrosine kinase inhibitors (TKIs). Despite well-defined guidelines to treat and monitor the disease, it is difficult to predict the occurrence of a sudden blast crisis. Research directed towards improving guidelines in choosing the appropriate TKIs and better monitoring protocols could help prevent such unfortunate outcomes. We present a case of a 46-year-old man diagnosed with CML who responded well to imatinib as evidenced by a downtrend in quantitative BCR-ABL mutation to less than 1. He quickly transformed into a blast crisis phase after five months of therapy with imatinib regardless of achieving an excellent initial optimal response. In conclusion, it is possible to transform into a blast phase despite achieving an initial optimal response. Therefore, attention should be focused on the selection of proper tyrosine kinase inhibitors and careful monitoring to allow the early detection of sudden blast crisis.