Working memory refers to a system for temporary storage and manipulation of information in the brain, a function critical for a wide range of cognitive operations. It has been proposed that working memory includes a central executive system (CES) to control attention and information flow to and from verbal and spatial short-term memory buffers. Although the prefrontal cortex is activated during both verbal and spatial passive working memory tasks, the brain regions involved in the CES component of working memory have not been identified. We have used functional magnetic resonance imaging (fMRI) to examine brain activation during the concurrent performance of two tasks, which is expected to engage the CES. Activation of the prefrontal cortex was observed when both tasks are performed together, but not when they are performed separately. These results support the view that the prefrontal cortex is involved in human working memory.

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These findings suggest that Ross syndrome is a dysautonomic condition of varying expression resulting from a generalized injury to ganglion cells or their projections.

BackgroundPrimary central nervous system lymphoma (PCNSL) may rarely be preceded by “sentinel demyelination,” a pathologic entity characterized by histologically confirmed demyelinating inflammatory brain lesions that mimic multiple sclerosis (MS) or acute disseminated encephalomyelitis (ADEM). Interpreting the overlapping radiologic and clinical characteristics associated with each of these conditions—contrast-enhancing demyelination of white matter and relapsing and remitting steroid-responsive symptoms respectively—can be a significant diagnostic challenge.Case presentationWe describe a 57-year-old woman with an unusual clinical course who presented with multi-focal enhancing white matter lesions demonstrated to be inflammatory demyelination by brain biopsy. Despite a good initial response to steroids and rituximab for treatment of presumed tumefactive multiple sclerosis, the patient’s condition rapidly deteriorated, and a repeat brain biopsy six months later was consistent with a diagnosis of diffuse large B-cell lymphoma.ConclusionsEarly clinical suspicion for PCNSL and awareness that biopsied lesions may initially show sentinel demyelination suggestive of alternate diagnoses may be essential for early initiation of appropriate therapies and mitigation of disease progression. Clinical, pathophysiological, and diagnostic aspects of sentinel demyelination and PCNSL are discussed.

Three children with acute lymphoblastic leukemia developed altered mental status, headaches, seizures, and visual changes associated with reversible posterior cerebral changes on MRI. These clinical and radiologic findings were consistent with the reversible posterior leukoencephalopathy syndrome, which has not been widely recognized in this setting.

Selective loss of all forms of saccades, with sparing of other eye movements, indicates malfunction of the brainstem machinery that generates saccades. A current model of brainstem circuits could account for both hypometria and slowing. This syndrome and the visual disability it causes often go unrecognized unless saccades are systematically tested at the bedside.

The risk model developed may help radiologists suggest the possibility of TON and prioritize ophthalmology consults. However, future external validation of this prediction model is necessary.

Hyperintensity of the optic nerve due to diffusion restriction can serve as a specific imaging marker of traumatic optic neuropathy. When paired with reduced ADC values, this finding may be an important surrogate for visual acuity.