A 41-year-old woman presented with refractory low back pain for the last 6 months. Neurologic examination was normal. Blood tests showed high erythrocyte sedimentation rate. A spine MRI (figure 1) disclosed involvement of the T12 vertebral body. There was hyperintense signal in T2-weighted sequence and multiple linear hypointense areas with cortical and radiated pattern resembling the brain parenchyma (the "mini brain" sign) (figure 2). Biopsy confirmed solitary plasmacytoma. Mini brain sign represents cortical thickening and is most likely caused by lytic lesions.1 The thickened struts resemble sulci in the brain, leading to a small brain appearance. 2,3 A "spoke-wheel" pattern has also been described. Mini brain sign is considered highly specific for solitary plasmacytoma.

Objective: To evaluate the role of the involvement of white matter tracts in huntingtin gene mutation patients as a potential biomarker of the progression of the disease. Methods: We evaluated 34 participants (11 symptomatic huntingtin gene mutation, 12 presymptomatic huntingtin gene mutation, and 11 controls). We performed brain magnetic resonance imaging to assess white matter integrity using diffusion tensor imaging, with measurement of fractional anisotropy. Results: We observed a significant decrease of fractional anisotropy in the cortical spinal tracts, corona radiate, corpus callosum, external capsule, thalamic radiations, superior and inferior longitudinal fasciculus, and inferior frontal-occipital fasciculus in the Huntington disease group compared to the control and presymptomatic groups. Reduction of fractional anisotropy is indicative of a degenerative process and axonal loss. There was no statistically significant difference between the presymptomatic and control groups. Conclusion: White matter integrity is affected in huntingtin gene mutation symptomatic individuals, but other studies with larger samples are required to assess its usefulness in the progression of the neurodegenerative process.

A 67-year-old woman presented with falls, cognitive impairment, mild upgaze palsy and parkinsonism for 3 years. A MRI was unremarkable. A PET-CT with fluorodeoxyglucose (FDG) disclosed reduced metabolism in thalami, midbrain and frontal cortex (Figure 1), suggesting progressive supranuclear palsy (PSP). Posterior MRI showed typical features observed in PSP (Figure 2). PSP is a neurodegenerative disease which affects brainstem and basal ganglia 1 . Early differentiation between PSP and other atypical parkinsonism is a challenge 1 . MRI abnormalities in PSP usually appear in advanced stages 2 . In PSP, PET-CT involves upper brainstem, caudate nuclei, insula cortices and frontal cortex 3,4 .

In a simplistic and succinct way, Liliequist membrane may be understood as a projection formed by an arachnoid membrane extending from the dorsum sellae to the mammillary bodies. In spite of being well known to neurosurgeons, many radiologists neither know this anatomical structure nor give importance to its study. The imaging evaluation of this membrane is feasible and may be interesting for a better preoperative planning; postoperative evaluation of third ventriculostomies; and understanding of suprasellar arachnoid cysts and perimesencephalic hemorrhage. The present article illustrates the anatomy of the membrane, with emphasis on imaging findings, besides describing its possible clinical and surgical implications.