corpus callosum
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2022 ◽  
Vol 17 (3) ◽  
pp. 816-820
Author(s):  
Dhara Rana ◽  
Sayali Kulkarni ◽  
Jamshed Zuberi ◽  
Fred Berlin

Author(s):  
Kyoko Ohashi ◽  
Carl M. Anderson ◽  
Alaptagin Khan ◽  
Michael L. Rohan ◽  
Elizabeth A. Bolger ◽  
...  

2022 ◽  
Vol 12 (1) ◽  
pp. 81
Author(s):  
Dae Hyun Kim ◽  
Hyunkoo Kang

This study investigated the changes in the structural connectivity of the bilateral hemispheres over time following a middle cerebral artery infarction. Eighteen patients in the subacute group and nine patients in the chronic group with mild upper extremity motor impairment (Fugl-Meyer motor assessment score for the upper limb > 43) following middle cerebral artery infarction were retrospectively evaluated in this study. All the patients underwent T1-weighted and diffusion tensor imaging. Tract-based statistical analyses of fractional anisotropy were used to compare the changes in the bilateral structural connectivity with those of age-matched normal controls. The corticospinal tract pathway of the affected hemisphere, corpus callosum, and corona radiata of the unaffected hemisphere had decreased structural connectivity in the subacute group, while the motor association area and anterior corpus callosum in the bilateral frontal lobes had increased structural connectivity in the chronic group. The bilateral hemispheres were influenced even in patients with mild motor impairment following middle cerebral artery infarction, and the structural connectivity of the bilateral hemispheres changed according to the time following the stroke.


2022 ◽  
Vol 48 (1) ◽  
Author(s):  
Jong Ho Cha ◽  
Jung-Sun Lim ◽  
Yong Hun Jang ◽  
Jae Kyoon Hwang ◽  
Jae Yoon Na ◽  
...  

Abstract Background Necrotizing enterocolitis (NEC) is a devastating disease in preterm infants with significant morbidities, including neurodevelopmental impairment (NDI). This study aimed to investigate whether NEC is associated with (1) brain volume expansion and white matter maturation using diffusion tensor imaging analysis and (2) NDI compared with preterm infants without NEC. Methods We included 86 preterm infants (20 with NEC and 66 without NEC) with no evidence of brain abnormalities on trans-fontanelle ultrasonography and magnetic resonance imaging at term-equivalent age (TEA). Regional brain volume analysis and white matter tractography were performed to study brain microstructure alterations. NDI was assessed using the Bayley Scales of Infant and Toddler Development-III (BSID-III) at 18 months of corrected age (CA). Results Preterm infants with NEC showed significantly high risk of motor impairment (odds ratio 58.26, 95% confidence interval 7.80–435.12, p < 0.001). We found significantly increased mean diffusivity (MD) in the splenium of corpus callosum (sCC) (p = 0.001) and the left corticospinal tract (p = 0.001) in preterm infants with NEC. The sCC with increased MD showed a negative association with the BSID-III language (p = 0.025) and motor scores (p = 0.002) at 18 months of CA, implying the relevance of sCC integrity with later NDI. Conclusion The white matter microstructure differed between preterm infants with and without NEC. The prognostic value of network parameters of sCC at TEA may provide better information for the early detection of NDI in preterm infants.


Author(s):  
Yasin Böcü ◽  
Hakan Karabağli ◽  
Mevlüt Özgür Taşkapilioğlu ◽  
Gökhan Ocakoğlu

2022 ◽  
Vol 26 (6) ◽  
pp. 4-15
Author(s):  
A. A. Smirnova ◽  
L. N. Prakhova ◽  
A. G. Ilves ◽  
N. A. Seliverstova ◽  
T. N. Reznikova ◽  
...  

Abstract. Despite a high prevalence of mild cognitive impairment (MCI), there are no accepted algorithms of diff erentiating the syndrome and the prognosis evaluation of later cognitive decline at this time. Objective. To identify biomarkers of poor prognosis in the various MCI types by optimizing neuropsychological examination in combination with MRI morphometry of brain structures. Patients and methods. We examined 45 patients (9 men, 36 women, mean age 72 ± 6.7 years) with MCI according to the modifi ed Petersen’s criteria and the DSM-5 criteria. All patients underwent the MMSE scale, the Detailed Neuropsychological Testing (DNT), which included a Ten Words Test (TWT), a “Double Test” (DT), a visual acuity test, a high-fi eld magnetic resonance imaging (MRI) of the brain with morphometry of cerebral structures (FreeSurfer, FSL). Results. According to the MMSE score, MCI were found in 26 (58%) patients. During the DNT, depending on the state of memory, 14 participants of the study identifi ed a non-amnestic type of MCI (na-MCI), 15 — an amnestic variant with impaired reproduction (ar-MCI), and 16 people — an amnestic type with a primary memory defect (apm-MCI). Volume changes of the anterior corpus callosum segment (CCA) were signifi cantly associated with the Immediate Recall after 4th reading and the Delayed Recall in the general MCI group (rho = 0.58; 0.58; p < 0.05) and the apmMCI group (rho = 0.6; 0.56; p < 0.05). Kruskal–Wallis Test showed that there were signifi cant group diff erences in the volumes of the CCA, right caudate nucleus, left cerebellar hemisphere cortex, posterior corpus callosum segment and left thalamus. At the same time, the fi rst three structures were combined into a set of informative features for differentiating the type of MCI based on the results of Forward stepwise Discriminant Analysis with a 77.3% accurate classifi cation rate (Wilks’s Lambda: 0.35962; approx. F (6.78) = 8.678, p < 0.001). ROC-analysis established the threshold values of the CCA volumes of ≤ 0.05% and the right caudate nucleus volumes of ≤ 0.23% (81.25% sensitivity in both cases; 62.1% and 60.7% specifi city; AUC 0.787 and 0.767; 95% CI 0.639–0.865 and 0.615–0.881; OR 7.1 and 6.7 (95% CI 1.6–30.6 and 1.6–29), associated with a memory defect in persons with MCI, while the ORs are 7.1 and 6.7 (95% CI 1.6–30.6 and 1.6–29), respectively. When both cerebral structures were included in the logit model, 88.6% classifi cation accuracy, 92.6% sensitivity, and 82.4% specifi city of the method were achieved. Conclusion. It has been demonstrated that classifying patients into the various types of MCI based on the data of memory function refl ected by the DNT and supplemented with MRI morphometry of the brain areas may be used as a sensitive and specifi c instrument for determining the category of patients with a high risk of Alzheimer’s disease. A neuropsychological profi le with a defect in primary memory, atrophic changes in anterior segment of the corpus callosum and the right caudate nucleus have been proposed as biomarkers of poor prognosis. Further longitudinal studies are necessary to clarify the proposed biomarkers of poor prognosis information and to detail the mechanisms of the neurodegenerative process.


2022 ◽  
Author(s):  
Kristin D Dahl ◽  
Hannah A Hathaway ◽  
Adam R Almeida ◽  
Jennifer Bourne ◽  
Tanya L Brown ◽  
...  

In the central nervous system (CNS), oligodendrocyte progenitor cells (OPCs) differentiate into mature oligodendrocytes to generate myelin, which is essential for normal nervous system function. OPC differentiation is driven by signaling pathways such as mTOR (Mechanistic Target of Rapamycin), which functions in two distinct complexes: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2), containing Raptor or Rictor respectively. In the current studies, mTORC2 signaling was selectively deleted from OPCs in PDGFRα-Cre X Rictorfl/fl mice. This study examined developmental myelination in male and female mice, comparing the impact of mTORC2 deletion in the corpus callosum and spinal cord. In both corpus callosum and spinal cord, Rictor loss in OPCs resulted in early reduction in myelin RNAs and some myelin proteins. However, these deficits rapidly recovered in spinal cord, where normal myelin abundance and thickness was noted at post-natal day 21 and 1.5 months. By contrast, the losses in corpus callosum resulted in severe hypomyelination, and increased unmyelinated axons. The current studies focus on uniquely altered signaling pathways following mTORC2 loss in developing oligodendrocytes. A major mTORC2 substrate is phospho-Akt-S473, which was significantly reduced throughout development in both corpus callosum and spinal cord at all ages measured, yet this had little impact in spinal cord. Loss of mTORC2 signaling resulted in decreased expression of actin regulators such as gelsolin in corpus callosum, but only minimal loss in spinal cord. The current study establishes a regionally-specific role for mTORC2 signaling in OPCs, particularly in the corpus callosum.


BMC Neurology ◽  
2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Mika Hayakawa ◽  
Tomoyasu Matsubara ◽  
Yoko Mochizuki ◽  
Chisen Takeuchi ◽  
Motoyuki Minamitani ◽  
...  

Abstract Background The detailed neuropathological features of patients with autosomal recessive hereditary spastic paraplegia with a thin corpus callosum (TCC) and SPG11 mutations are poorly understood, as only a few autopsies have been reported. Herein, we describe the clinicopathological findings of a patient with this disease who received long-term care at our medical facility. Case presentation A Japanese man exhibited a mild developmental delay in early childhood and intellectual disability, followed by the appearance of a spastic gait by age 13. At the age of 25 years, he became bedridden and needed a ventilator. Genetic analysis revealed a homozygous splice site variant in the SPG11 gene (c. 4162–2A > G) after the provision of genetic counselling and acquisition of informed consent from his parents. He died of pneumonia at the age of 44. His brain weighed 967 g and was characterized by a TCC, and his spinal cord was flattened. Microscopically, degeneration was observed in the posterior spinocerebellar tract, the gracile fasciculus, and the posterior column in addition to the corticospinal tract. Marked neuronal loss and gliosis were observed in the anterior horn, Clarke’s column, and hypoglossal and facial nuclei. Various types of neurons, in addition to motor neurons, showed coarse eosinophilic granules that were immunoreactive for p62. The loss of pigmented neurons with gliosis was apparent in both the substantia nigra and locus coeruleus. Lateral geniculate body degeneration was a characteristic feature of this patient. Furthermore, peripheral Lewy body-related α-synucleinopathy and scattered α-synuclein–immunoreactive neurites in the locus coeruleus and reticular formation of the brainstem were observed. Conclusions In patients with hereditary spastic paraplegia with SPG11 mutations, a variety of clinical phenotypes develop due to widespread lesions containing p62-immunoreactive neuronal cytoplasmic inclusions. We herein report the lateral geniculate body as another degenerative site related to SPG11-related pathologies that should be studied in future investigations.


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