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Psychosocial Aspects of Diabetes
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
The signs and symptoms include disorientation, confusion, memory failure, restlessness, agnosia, speech disturbances, and difficulty with concentration and/or multitasking. Paranoia may be observed, such as in accusations of stealing or being threatened by others. Psychotic symptoms may be hallucinations or delusions. The patient may become verbally or physically aggressive. Patients are initially unable to handle complex daily tasks such as managing medications and finances, and driving. As the condition advances, they begin to have trouble completing more basic tasks such as feeding, dressing, toileting, or bathing. The majority of them must be moved to skilled nursing facilities with 24-hour care. The signs and symptoms may correlate with the location of brain atrophy. In AD, the parietal and temporal lobes are primarily affected. Therefore, memory and visuospatial task abnormalities are observed first. Language is preserved early in the disease until later stages.
Disorders Affecting White and Gray Matter:
Published in Swati Goyal, Neuroradiology, 2020
Generalized brain atrophy in later stages SWI − susceptibility artifact in the area of iron accumulationMRS − reduced NAA peak and elevated myo-inositol peak
Hematopoietic Stem Cell Transplantation for Multiple Sclerosis
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Athanasios Fassas, Richard K. Burt
An analysis of the first 10 patients performed at a median follow-up of 15 months (range, 4-30)14 showed that the enhancing activity began to decrease after cyclophosphamide mobilization and the number of lesions was zero in all patients after transplantation from 341 detected before mobilization. The number of T2-weighted positive lesions was also reduced: no new T2 lesions were observed in 9 of 10 patients after transplant, whereas 62 new lesions were detected during the three months of the pre-treatment period. In a recent update of this study, brain atrophy was still present and ongoing at one year, but it appeared to slow down after the 6th month. Oligoclonal bands were still detected in CSF at 2 years after HSCT. Clinically, the patients were stable or slightly improved.15 No major adverse events were recorded except for a case of hemorrhagic cystitis after cyclophosphamide. After transplant, CMV reactivation occurred in 5 cases, one symptomatic, and zoster developed in two cases. Infections or fever were common in the early period, as was transient worsening of the previous neurological condition.
Central nervous system involvement in two siblings affected by hereditary transthyretin amyloidosis 30 years after liver transplantation: a model for gene-silencing therapies
Published in Neurological Research, 2023
A Di Paolantonio, A Romano, V Guglielmino, F Vitali, MA Sciarrone, G Bisogni, T Verdolotti, M Maceroni, AM Minnella, M Luigetti
Once understood the pathogenesis of ATTRv, that is the deposit in tissues of an unstable transthyretin produced mainly by the liver, OLT was proposed as the best treatment option, especially in young patients. After the first transplant in 1990, several studies assessed patient clinical outcomes, demonstrating really satisfactory results in survival and stabilization of neuropathy and cardiomyopathy, more in V30M early-onset patients than in non-V30M [15]. However, liver transplant would not completely halt disease progression. As already mentioned, a significant amount of mutated protein would still be produced by the choroid plexus in the brain, depositing in leptomeningeal tissues and vessels. One case here described suffered effectively from recurrent aphasic episodes. Surprisingly, his brain was normal on MRI evaluation. We hypothesize that some so-called ‘amyloid spells’ had occurred: they are TIA-like episodes without frank brain focal lesions on MRI that are common in patients with a known amyloid angiopathy [17]. The occurrence of these events in ATTRv patients makes a bridge with patients with degenerative brain amyloidosis, both sharing cognitive degeneration and stroke-like episodes. On the opposite, some brain alterations were found in Case 2, despite a clinical history free from central nervous system symptoms. We think that a sum of numerous subclinical events due to progressive brain amyloid deposition is the cause of brain atrophy in our patient.
On diagnostic accuracy measure with cut-points criterion for ordinal disease classification based on concordance and discordance
Published in Journal of Applied Statistics, 2023
Jing Kersey, Hani Samawi, Jingjing Yin, Haresh Rochani, Xinyan Zhang
Figure 4 presents five core biomarkers as indicators of AD over the clinical disease stages. The curves depict changes from normal to abnormal in the following five biomarkers [20] over AD's progression. FDG-PET measures tau protein in cerebrospinal fluid or by synaptic dysfunction.Brain atrophy measured by structural MRI.Cognitive tests measure memory loss.Cognitive testsmeasure clinical function.
An investigation of cerebral bridging veins rupture due to head trauma
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2023
Hamed Abdi, Kamran Hassani, Shahrokh Shojaei
In this study, we examined whether brain atrophy and age affect the amount of BV damage that can cause a subdural hematoma. For this purpose, using numerical modeling, two sets of models including healthy and atrophied brains were created and their results were compared. The results of global solid models showed that relative displacement, between skull and brain, was more common in atrophied models. Therefore, the risk of impact damage was in people with brain atrophy. On the other hand, the pressure was more on the atrophied model due to head impact. Moreover, the strains of the BVs were more in atrophied models caused by the high amount of relative motion between skull and brain. When head impact with a HIC value of 740 was applied to the healthy and atrophic model, we showed that this loading was not strong enough to cause severe injuries to the young human with a healthy brain. But this impact was strong enough to lead to severe injury in the old human with an atrophied brain. In previous studies, the results could not be referred to all humans because the effects of brain atrophy were not considered. Here, we tried to introduce a model that considered the effects of aging and associated brain atrophy for more reliable results.