scholarly journals Structural reorganization of the white matter pathways of the brain in patients with spastic diplegia after translingual neurostimulation

2021 ◽  
Vol 8 (4) ◽  
pp. 27-34
Author(s):  
K. S. Anpilogova ◽  
D. S. Chegina ◽  
T. S. Ignatova ◽  
A. Yu. Efimtsev ◽  
G. E. Trufanov
Keyword(s):  
White Matter ◽  
Motor Skills ◽  
Structural Changes ◽  
Muscle Tone ◽  
Controlled Study ◽  
Cerebral White Matter ◽  
Spastic Diplegia ◽  
Functional Impairments ◽  
The Brain ◽  
Stimulation Of

Background. Spastic diplegia (Little’s disease) is the most common form of infantile cerebral palsy (ICP), leading to persistent motor and functional impairments. One promising area of rehabilitation is a combination of physical therapy with methods of stimulation of various parts of the nervous system, among which functional electrical stimulation of muscles and nerves is the most prominent.Objective. To study structural changes of cerebral white matter conduction pathways in patients with spastic diplegia after translingual neurostimulation using magnetic resonance tractography.Materials and Methods. An open single center-controlled study was conducted. A total of 18 children were examined. All patients underwent comprehensive MRI in two time points, before and after a course of translingual neurostimulation, on a tomograph with magnetic field induction 3.0 Tesla, which included a traditional protocol in 3 mutually perpendicular planes), and diffusion-weighted imaging — DWI (Diffusion-Weight Imaging).Results. All patients after neurostimulation showed clinical improvement of movement coordination and decrease of muscle tone with formation of new motor skills, improvement of limb motor function. Statistically significant decrease of spasticity index was revealed up to 17% for arms and 23% for legs, improvement of motor skills on all three scales.Conclusion. Translingual neurostimulation allows to affect all components of motor activity, as a result of which neuroplasticity processes are activated and the brain of patients with spastic diplegia becomes more receptive to motor rehabilitation aimed at restoration of motor control and formation of new motor skills.

scholarly journals Relationship Between Type 2 Diabetes and White Matter Hyperintensity: A Systematic Review

2020 ◽  
Vol 11 ◽  
Author(s):  
Dan-Qiong Wang ◽  
Lei Wang ◽  
Miao-Miao Wei ◽  
Xiao-Shuang Xia ◽  
Xiao-Lin Tian ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
White Matter ◽  
Structural Changes ◽  
White Matter Lesions ◽  
Poor Performance ◽  
White Matter Hyperintensity ◽  
Diabetic Microangiopathy ◽  
The Relationship ◽  
The Brain

White matter (WM) disease is recognized as an important cause of cognitive decline and dementia. White matter lesions (WMLs) appear as white matter hyperintensities (WMH) on T2-weighted magnetic resonance imaging (MRI) scans of the brain. Previous studies have shown that type 2 diabetes (T2DM) is associated with WMH. In this review, we reviewed the literature on the relationship between T2DM and WMH in PubMed and Cochrane over the past five years and explored the possible links among the presence of T2DM, the course or complications of diabetes, and WMH. We found that: (1) Both from a macro- and micro-scopic point of view, most studies support the relationship of a larger WMH and a decrease in the integrity of WMH in T2DM; (2) From the relationship between brain structural changes and cognition in T2DM, the poor performance in memory, attention, and executive function tests associated with abnormal brain structure is consistent; (3) Diabetic microangiopathy or peripheral neuropathy may be associated with WMH, suggesting that the brain may be a target organ for T2DM microangiopathy; (4) Laboratory markers such as insulin resistance and fasting insulin levels were significantly associated with WMH. High HbA1c and high glucose variability were associated with WMH but not glycemic control.

Neurotrophins in the brain of C57BL/6-Plautm1.1BugThisPlauGFDhu/GFDhu mice with B16/F10 melanoma growing with comorbid pathology.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e21557-e21557
Author(s):  
Elena M. Frantsiyants ◽  
Irina V. Kaplieva ◽  
Valeria A. Bandovkina ◽  
Ekaterina I. Surikova ◽  
Irina V. Neskubina ◽  
...  
Keyword(s):  
White Matter ◽  
Tumor Growth ◽  
Tumor Volume ◽  
Gene Knockout ◽  
Chronic Neuropathic Pain ◽  
Inhibition Of Tumor Growth ◽  
Growth Changes ◽  
The Brain ◽  
Melanoma Growth ◽  
Stimulation Of

e21557 Background: 10% of cancer patients have comorbidities accompanied by chronic pain. Neurotrophins and fibrinolytic system are involved in carcinogenesis and pain pathogenesis. The purpose of the study was to measure levels of neurotrophins in white matter of the brain of urokinase-deficient (uPA–) mice with B16/F10 melanoma growing in presence of chronic neuropathic pain (CNP). Methods: The study included female mice С57ВL/6 (normal genome uPA+, n = 40) and C57BL/6-Plautm1.1BugThisPlauGFDhu/GFDhu (urokinase gene-knockout uPA–, n = 28) with B16/F10 melanoma (M) implanted subcutaneously 2 weeks after bilateral sciatic nerve ligation (CNP model). Intact mice (I) were controls. Levels of brain-derived neurotrophic factor BDNF, nerve growth factor NGF-β and neurotrophins 3 and 4 (NT3, NT4) were measured by ELISA in white matter of the brain after 3 weeks of tumor growth in presence of CNP. Results: Tumor volume in (uPA–) females by week 3 of carcinogenesis was 0.04 cm3, which was 70 times smaller than in (uPA+) females. Tumor volume in (uPA–) females with CNP was 5.76 cm3, which was 144 times larger than in (uPA–) females without CNP, and in (uPA+) females – 2.5 cm3. The brain of I (uPA–) showed higher levels of NT3 (by 1.3 times, p < 0.05), NT4 (by 2.6 times) and NGF-β (by 1.9 times, p < 0.05) and lower BDNF (by 1.7 times, p < 0.05), compared to I (uPA+). Both strains of mice with M or CNP demonstrated decreased levels of NGF-β, more pronounced in animals with a combination of these factors. (uPA–) females with CNP+M showed a decrease of NT3 and BDNF by 2 times, with NGF-β 2.2 times higher than in (uPA+) mice. Conclusions: The study revealed underlying differences in levels of neurotrophins in the brain of (uPA–) females which could contribute to the creation of conditions for the inhibition of tumor growth. Changes in the levels of NGF-β in mice with melanoma or CNP were nonspecific. Changes in the BDNF, NT3 and NGF-β balance in the brain of (uPA–) mice may be part of the mechanism of greater stimulation of melanoma growth under the influence of CNP.

scholarly journals Connecting Cerebral White Matter Lesions and Hypertensive Target Organ Damage

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Cristina Sierra ◽  
Alfons López-Soto ◽  
Antonio Coca
Keyword(s):  
Risk Factor ◽  
White Matter ◽  
Brain Damage ◽  
White Matter Lesions ◽  
Organ Damage ◽  
Left Ventricular ◽  
Cerebral White Matter ◽  
Chronic Hypertension ◽  
Cerebral White Matter Lesions ◽  
The Brain

Chronic hypertension leads to concomitant remodeling of the cardiac and vascular systems and various organs, especially the brain, kidney, and retina. The brain is an early target of organ damage due to high blood pressure, which is the major modifiable risk factor for stroke and small vessel disease. Stroke is the second leading cause of death and the number one cause of disability worldwide and over 80% of strokes occur in the elderly. Preclinical hypertensive lesions in most target organs are clearly identified: left ventricular hypertrophy for the heart, microalbuminuria for the kidney, fundus abnormalities for the eye, and intima-media thickness and pulse wave velocity for the vessels. However, early hypertensive brain damage is not fully studied due to difficulties in access and the expense of techniques. After age, hypertension is the most-important risk factor for cerebral white matter lesions, which are an important prognostic factor for stroke, cognitive impairment, dementia, and death. Studies have shown an association between white matter lesions and a number of extracranial systems affected by high BP and also suggest that correct antihypertensive treatment could slow white matter lesions progression. There is strong evidence that cerebral white matter lesions in hypertensive patients should be considered a silent early marker of brain damage.

The Cerebrum, Cerebellum, & Cognitive Disorders

Neuroanatomy ◽  
2017 ◽  
pp. 287-340
Author(s):  
Adam J Fisch
Keyword(s):  
White Matter ◽  
Cognitive Disorders ◽  
Sylvian Fissure ◽  
Arterial Supply ◽  
Cerebral White Matter ◽  
Brodmann Areas ◽  
Cerebellar Peduncles ◽  
Key Features ◽  
The Brain ◽  
Cerebellar Disorders

This chapter focuses on the cerebral lobes and some additional key features of the superior and inferior surfaces of the brain, as well as on the structures of the cerebellum. Instructions are provided on how to draw the multiple lobes and surfaces of the cerebrum, gyri, sulci, insula, Sylvian fissure, Brodmann areas, neocortical layers, cerebellum, cerebellar peduncles, the corticopontocerebellar pathway, cerebellar midline structures, arterial supply, cerebral white matter, and commissural fibers. Also discussed are features of histology of neurons and glia and cerebellar histology. Cerebral and cerebellar disorders are also presented, including cognitive disorders, apraxia, and neglect.

scholarly journals Chemotherapy-induced structural changes in cerebral white matter and its correlation with impaired cognitive functioning in breast cancer patients

2011 ◽  
Vol 32 (3) ◽  
pp. 480-493 ◽  
Author(s):  
Sabine Deprez ◽  
Frederic Amant ◽  
Refika Yigit ◽  
Kathleen Porke ◽  
Judith Verhoeven ◽  
...  
Keyword(s):  
Breast Cancer ◽  
White Matter ◽  
Cognitive Functioning ◽  
Cancer Patients ◽  
Structural Changes ◽  
Cerebral White Matter ◽  
Breast Cancer Patients
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