The Neuroimaging Spectrum of Septum Posticum Derangement and Associated Thoracic Myelopathy.

BACKGROUND: Arachnoid cysts and meningeal membranes are among the differential diagnostic considerations of extra-medullary causes of thoracic myelopathy. In this case series of 7 patients, we present compressive meningeal membranes mimicking dorsal arachnoid cyst. The propensity of the meningeal membranes for the dorsal aspect of upper thoracic spine may reflect derangements of the septum posticum. OBJECTIVE: To provide the spectrum of imaging appearances and clinical presentations of pathology of the septum posticum to improve imaging utilization and to better guide treatment planning. METHODS: Seven patients aged 40 to 75 with MRI findings of ventral displacement and dorsal cord compression in the upper thoracic spine were further evaluated with CT-myelograms. The primary indication was to exclude dorsal arachnoid cyst. Two patients with progressive symptoms and lower extremity weakness were operated for decompression. RESULTS: CT-myelogram excluded space occupying lesions and cord herniation in all cases. Intradural dorsal meningeal webs and membranes were inconsistently visualized. In the 2 operated cases, thick coalescing membranes and hyperdynamic turbulent CSF flow were severely compressing the thoracic cord. CONCLUSION: Derangements of septum posticum may present a spectrum of findings that should be considered in the differential of thoracic myelopathy. Flattening of the posterior cord margin is a reliable imaging clue for a dorsal extra-medullary compressive lesion. Cord compression results from combination of adhesive membranes and turbulent CSF flow. The clinical course may be difficult to predict. Periodic imaging follow up can be helpful to confirm stability of findings in expectantly managed cases.

T2 hyperintensity of medial lemniscus: higher threshold application to ROI measurements is more accurate in predicting small vessel disease.

BACKGROUND: Medial lemniscus T2 hyperintensity (MLH) has been recently demonstrated as potential imaging marker for small vessel disease (SVD). Our purpose in this study is to improve accuracy of regions of interest (ROI) analysis for this imaging finding. METHODS AND METHODS: Two neuroradiologists retrospectively reviewed 103 consecutive outpatient brain MRI. Medial lemniscus signal in dorsal pons was evaluated; visually on FLAIR and with ROI on T2. Original MRI interpretations were divided into three categories; SVD, multiple sclerosis (MS), and nonspecific WM changes (non). RESULTS: Thirty-seven patients had SVD, 14 patients had MS, 52 had Non. Visual MLH was seen exclusively with SVD and was generally bilateral. Patients with visual MLH belonged to advanced SVD by imaging and clinical parameters. Compared to visual data, ROI analyses of MLH has been known to be compounded by false positives and negatives at low threshold (20% of adjacent to normal brainstem signal). With application of higher ROI threshold (25%), false positives were eliminated but false negatives increased. ROI analyses of MLH by experienced neuroradiologist were more reliable. CONCLUSION: MLH seen on high threshold ROI analysis is a reliable radiologic marker in predicting SVD. ROI analysis of MLH should be performed by an experienced neuroradiologist.

Brain-derived neurotrophic factor does not influence age at neurologic onset of Huntington's disease.

In Huntington's disease (HD), genetic factors in addition to the HD CAG repeat mutation play a significant role in determining age at neurologic onset. Brain-derived neurotrophic factor (BDNF), a survival factor for striatal neurons, has been implicated as a target of regulation by huntingtin and is an attractive candidate as a genetic modifier. We tested this hypothesis by genotyping a SNP known to alter BDNF function (rs6265, also termed Val66Met) and a SNP associated with Alzheimer disease (BDNF C270T), along with two BDNF intronic SNPs (rs7103411, rs11030104), in 228 cases with extreme young onset and 329 cases with extreme old onset of HD. No differences were seen between groups for allele frequencies or genotype frequencies for any SNP. Furthermore, no association to onset age was seen in GEE models controlling for HD repeat size or in haplotype analyses of these SNPs. These results indicate that BDNF does not influence significantly the mechanisms in HD pathogenesis that lead to neurologic onset.