No abstract

A 79-year-old man experienced cognitive impairment and visual field defects during ofatumumab therapy for chronic lymphocytic leukemia refractory to combination chemotherapy. Magnetic resonance imaging revealed T1-weighted low-intensity and T2-weighted high-intensity lesions with patchy gadolinium enhancement in the subcortical white matter. A diagnosis of progressive multifocal leukoencephalopathy was made after the detection of John Cunningham virus (JCV) DNA in his cerebrospinal fluid (CSF). Following plasma exchange and the administration of mirtazapine and mefloquine, the JCV DNA levels in the CSF decreased. However, the patient died 55 days after treatment was initiated. Ofatumumab treatment appears to be associated with the development of PML.

A 19-year-old man with a history of Chiari type I malformation was admitted to our hospital two times within a 2month period because of bacterial meningitis. Cerebrospinal fluid (CSF) analysis showed neutrophilic pleocytosis and hypoglycorrhachia. During the second admission, we became aware of hearing loss on the right since age 15 years. Highresolution temporal bone CT showed soft tissue opacification of the right epitympanum and external auditory canal. Tissue biopsy resulted in CSF otorrhea and pneumocephalus. CT cisternography revealed a temporal bone CSF leak. Brain MRI showed a dural defect localized to the anterior petrous apex. Using a combined middle cranial fossatransmastoid approach, the dural defect and associated arachnoid granulations were located along the superior side of the greater petrosal nerve and repaired. A CSF leak without underlying pathology, such as trauma, surgery, or congenital abnormality, is defined as spontaneous. Spontaneous CSF leak should be considered as a cause of recurrent bacterial meningitis even when CSF otorrhea and fluid behind the tympanic membrane are clinically absent.