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Impact of brain atrophy on 90-day functional outcome after moderate-volume basal ganglia hemorrhage.

ABSTRACT: This study aimed to evaluate the effect of brain atrophy on the functional outcome of patients with moderate-volume basal ganglia hemorrhage. Of 1003 patients with spontaneous intracerebral hemorrhage, 124 with moderate-volume basal ganglia hemorrhage (hematoma volume of 20-50?mL) were enrolled. The intercaudate distance (ICD) and sylvian fissure ratio (SFR) were used as linear brain atrophy parameters. The patients were divided into groups with favorable and unfavorable outcomes, according to the Glasgow Outcome Scale score, 90 days after symptom onset. Demographic and radiographic features, including the ICD and SFR, were compared between the two groups. Among the 124 patients, 74 (59.7%) exhibited a favorable outcome. The ICD and SFR values were significantly greater for the favorable group than for the unfavorable group. Multivariate analysis indicated that young age, high Glasgow Coma Scale score at admission, small hematoma volume, and increased ICD (odds ratio [OR], 1.207; 95% confidence interval [CI], 1.004-1.451) and SFR (OR, 1.046; 95% CI, 1.007-1.086, per 0.001) values had a beneficial effect on functional outcome. In conclusion, brain atrophy exhibits protective effects in patients with moderate-volume basal ganglia hemorrhage, and is an important factor for predicting functional outcome.

SUBMITTER: Kwon SM

PROVIDER: S-EPMC5859038 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature

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Impact of brain atrophy on 90-day functional outcome after moderate-volume basal ganglia hemorrhage.

Kwon Sae Min SM Choi Kyu-Sun KS Yi Hyeong-Joong HJ Ko Yong Y Kim Young-Soo YS Bak Koang-Hum KH Chun Hyoung-Joon HJ Lee Young-Jun YJ Lee Ji Young JY

Scientific reports 20180319 1

This study aimed to evaluate the effect of brain atrophy on the functional outcome of patients with moderate-volume basal ganglia hemorrhage. Of 1003 patients with spontaneous intracerebral hemorrhage, 124 with moderate-volume basal ganglia hemorrhage (hematoma volume of 20-50 mL) were enrolled. The intercaudate distance (ICD) and sylvian fissure ratio (SFR) were used as linear brain atrophy parameters. The patients were divided into groups with favorable and unfavorable outcomes, according to t ...[more]

PMID: 29555930

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Project description:Huntington's disease is caused by a CAG repeat expansion in the Huntingtin gene (HTT), coding for polyglutamine in the Huntingtin protein, with longer CAG repeats causing earlier age of onset. The variable 'Age' × ('CAG'-L), where 'Age' is the current age of the individual, 'CAG' is the repeat length and L is a constant (reflecting an approximation of the threshold), termed the 'CAG Age Product' (CAP) enables the consideration of many individuals with different CAG repeat expansions at the same time for analysis of any variable and graphing using the CAG Age Product score as the X axis. Structural MRI studies have showed that progressive striatal atrophy begins many years prior to the onset of diagnosable motor Huntington's disease, confirmed by longitudinal multicentre studies on three continents, including PREDICT-HD, TRACK-HD and IMAGE-HD. However, previous studies have not clarified the relationship between striatal atrophy, atrophy of other basal ganglia structures, and atrophy of other brain regions. The present study has analysed all three longitudinal datasets together using a single image segmentation algorithm and combining data from a large number of subjects across a range of CAG Age Product score. In addition, we have used a strategy of normalizing regional atrophy to atrophy of the whole brain, in order to determine which regions may undergo preferential degeneration. This made possible the detailed characterization of regional brain atrophy in relation to CAG Age Product score. There is dramatic selective atrophy of regions involved in the basal ganglia circuit-caudate, putamen, nucleus accumbens, globus pallidus and substantia nigra. Most other regions of the brain appear to have slower but steady degeneration. These results support (but certainly do not prove) the hypothesis of circuit-based spread of pathology in Huntington's disease, possibly due to spread of mutant Htt protein, though other connection-based mechanisms are possible. Therapeutic targets related to prion-like spread of pathology or other mechanisms may be suggested. In addition, they have implications for current neurosurgical therapeutic approaches, since delivery of therapeutic agents solely to the caudate and putamen may miss other structures affected early, such as nucleus accumbens and output nuclei of the striatum, the substantia nigra and the globus pallidus.

Dataset Information

Impact of brain atrophy on 90-day functional outcome after moderate-volume basal ganglia hemorrhage.

Publications

Impact of brain atrophy on 90-day functional outcome after moderate-volume basal ganglia hemorrhage.

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