Structural MRI is widely used for investigating brain atrophy in many neurodegenerative disorders, with several research groups developing and publishing techniques to provide quantitative assessments of this longitudinal change. Often techniques are compared through computation of required sample size estimates for future clinical trials. However interpretation of such comparisons is rendered complex because, despite using the same publicly available cohorts, the various techniques have been assessed with different data exclusions and different statistical analysis models. We created the MIRIAD atrophy challenge in order to test various capabilities of atrophy measurement techniques. The data consisted of 69 subjects (46 Alzheimer's disease, 23 control) who were scanned multiple (up to twelve) times at nine visits over a follow-up period of one to two years, resulting in 708 total image sets. Nine participating groups from 6 countries completed the challenge by providing volumetric measurements of key structures (whole brain, lateral ventricle, left and right hippocampi) for each dataset and atrophy measurements of these structures for each time point pair (both forward and backward) of a given subject. From these results, we formally compared techniques using exactly the same dataset. First, we assessed the repeatability of each technique using rates obtained from short intervals where no measurable atrophy is expected. For those measures that provided direct measures of atrophy between pairs of images, we also assessed symmetry and transitivity. Then, we performed a statistical analysis in a consistent manner using linear mixed effect models. The models, one for repeated measures of volume made at multiple time-points and a second for repeated “direct” measures of change in brain volume, appropriately allowed for the correlation between measures made on the same subject and were shown to fit the data well. From these models, we obtained estimates of the distribution of atrophy rates in the Alzheimer's disease (AD) and control groups and of required sample sizes to detect a 25% treatment effect, in relation to healthy ageing, with 95% significance and 80% power over follow-up periods of 6, 12, and 24 months. Uncertainty in these estimates, and head-to-head comparisons between techniques, were carried out using the bootstrap. The lateral ventricles provided the most stable measurements, followed by the brain. The hippocampi had much more variability across participants, likely because of differences in segmentation protocol and less distinct boundaries. Most methods showed no indication of bias based on the short-term interval results, and direct measures provided good consistency in terms of symmetry and transitivity. The resulting annualized rates of change derived from the model ranged from, for whole brain: − 1.4% to − 2.2% (AD) and − 0.35% to − 0.67% (control), for ventricles: 4.6% to 10.2% (AD) and 1.2% to 3.4% (control), and for hippocampi: − 1.5% to − 7.0% (AD) and − 0.4% to − 1.4% (control). There were ...
BackgroundAs cognitive impairment increases with age, sulcal atrophy (SA) and the enlargement of the ventricles also increase. Considering the measurements on the previously proposed visual scales, a new scale is proposed in this study that allows us to evaluate the atrophy, white matter hyperintensities (WMHs), basal ganglia infarct (BGI), and infratentorial infarct (ITI) together. Our aim of this study is to propose a practical and standardized MRI for the clinicians to be used in daily practice.MethodsA total of 97 patients older than 60 years and diagnosed with depression or Alzheimer’s disease (AD) are included. Cranial MRI, Mini Mental State Examination (MMSE), detailed neuropsychometric tests, and depression scales are applied to all patients. The SA, ventricular atrophy (VA), medial temporal lobe atrophy (MTA), periventricular WMH (PWMH), subcortical WMH (SCWMH), BGI, and ITI are scored according to the scale. The total score is also recorded.ResultsThe average age of the patients was 74.53, and the mean MMSE score was 22.7 in the degenerative group and 27.8 in the non-degenerative group. Among the patients, 50 were diagnosed with AD. All parameters significantly increased with age. In the degenerative group, SA, VA, MTA, PWMH, SCWMH, and total scores were found to be significantly higher. Sensitivities of VA, PWMH, SCWMH, and total scores, as well as both sensitivity and specificities of MTA score, were observed to be high. When they were combined, sensitivities and specificities were found to be high.ConclusionThe scale is observed to be predictive in discriminating degenerative and non-degenerative processes. This discrimination is important, particularly in depressive patients complaining of forgetfulness.
Juvenile myoclonic epilepsy (JME) is hypothesized to originate from the dysfunction of thalamo-cortical circuit. We aimed to analyze any changes in auditory startle response in JME patients to determine the role of brainstem in JME. The responses of 18 JME patients to auditory simulation were recorded over the unilateral orbicularis oculi, masseter, sternocleidomastoid, and extremity muscles. Results were compared with those of 18 age and gender matched healthy volunteers. Total auditory startle response frequencies were similar between the two groups (31.1 ± 11.1 % vs. 33.7 ± 8.7 %, p = 0.400). Other parameters over each muscle were also similar. There were no impacts of antiepileptic drug use or disease duration. We may conclude that our findings may provide sufficient evidence for the lack of functional changes of the auditory startle response circuit even in longstanding cases of JME.
Background: Reversible posterior leukoencephalopathy syndrome (RPLS) is a clinicoradiologic syndrome characterized by headache, decreased alertness, seizures, visual abnormalities, and white matter changes indicative of cerebral edema. Although the pathogenesis remains poorly understood, several etiological causes have been described. RPLS is a common complication of chemotherapeutics because of its toxic effect on the central nervous system. This syndrome is frequently associated with seizures but rarely seen with status epilepticus and periodic lateralized epileptiform discharges (PLEDs). Case Report:We present a case with metastatic lung cancer that developed RPLS after carboplatin and paclitaxel therapy. Our case was admitted to the hospital with status epilepticus and her electroencephalography showed PLEDs. Conclusion: It is important to closely monitor blood pressure and electrolyte levels in patients who take chemotherapeutic agents, especially when there is no previous history of hypertension. It should be kept in mind that RPLS is a causative factor of status epilepticus and PLEDs.
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