Introduction:There is conflicting data on the risk factors for recurrent lumbar disc herniation (rLDH). Most of the predictors for rLDH identified so far are acquired risk factors or radiological factors at the level of the herniation. Whole lumbar spine (WLS) morphometry has not been evaluated as a possible predictor of rLDH.Objectives:We aimed to evaluate if preoperative spinal morphometry can predict the occurrence of rLDH requiring revision surgery.Methods:This retrospective case-control study on 250 patients included 45 patients operated for rLDH, 180 controls without rLDH who had previously undergone microdiscectomy for a single level lumbar disc prolapse, and a holdout validation set of 25 patients. Morphometric variables related to the WLS were recorded in addition to previously identified predictors of rLDH. Logistic regression (LR) analysis was performed to identify independent predictors of rLDH.Results:LR yielded four predictors of which two were WLS morphometric variables. While increasing age and smoking positively predicted rLDH, increasing WLS interfacet distance and WLS dural-sac circumference negatively predicted rLDH. The LR model was statistically significant, χ2(4) =15.98,P= 0.003, and correctly classified 80.3% of cases. On validation, the model demonstrated a fair accuracy in predicting rLDH (accuracy: 0.80, AUC: 0.70).Conclusions:Larger mean lumbar bony canals and dural sacs protect from the occurrence of symptomatic rLDH. These WLS morphometric variables should be included in future risk stratification algorithms for lumbar disc disease. In addition to the previously recognized risk factors, our study points to an underlying developmental predisposition for rLDH.
Background:
Huntington's disease (HD) is a progressive neurodegenerative disorder characterized by motor, cognitive, and psychiatric abnormalities. Currently, matched analyses of structural and functional differences in the brain from the same study cohort and, specifically, in HD patients from an ethnically diverse Indian population are lacking. Such findings aid in identifying noninvasive and sensitive imaging biomarkers.
Objective:
The aim of the study was to understand the structural and functional differences between HD and control brain, and presymptomatic and symptomatic HD brain in the Indian population.
Materials and Methods:
Seventeen HD (11 symptomatic HD [S-HD] and six presymptomatic HD [P-HD], with comparable CAG repeats), and 12 healthy controls were examined. Macrostructural (volume), microstructural (diffusivity), and functional (neurochemical levels and glucose metabolism) imaging of the brain was done along with the determination of visual latencies.
Results:
HD brain showed increased intercaudate distance; significant subcortical volumetric loss; reduced fractional anisotropy; increased mean, axial, and radial diffusivity; lower levels of total N-acetyl aspartate; elevated total choline levels; and reduced glucose metabolism compared with control brain. Interestingly, compared with P-HD, S-HD patients demonstrated a strong inverse correlation between age at onset and CAG repeat length, and prolonged P100 latency. In addition, caudate and putamen in S-HD brain showed significant volumetric loss and increased diffusivity compared with P-HD brain.
Conclusions:
HD brain showed distinct macrostructural, microstructural, and functional differences compared with control brain in the Indian population. Interestingly, patients with S-HD had a significant volumetric loss, increased diffusivity, altered neurochemical profile, and delayed P100 latency compared with P-HD patients. Examining these alterations clinically could aid in monitoring the progression of HD.
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