Data quality in diffusion tensor imaging studies of the preterm brain: a systematic review

Background: To study early neurodevelopment in preterm infants, evaluation of brain maturation and injury is increasingly performed using diffusion tensor imaging, for which the reliability of underlying data is paramount. Objective: To review the literature to eva

Cerebello-cerebral connectivity in the developing brain

Disrupted cerebellar development and injury is associated with impairments in both motor and non-motor domains. Methods to non-invasively characterize cerebellar afferent and efferent connections during early development are lacking. The aim of this study was to assess the feasibility of delineating cortico-ponto-cerebellar (CPC) and cerebello-thalamo-cortical (CTC) white matter tracts during brain development using high angular resolution diffusion imaging (HARDI). HARDI data were obtained in 24 infants born between 24+6 and 39 weeks gestational age (median 33+4 weeks) and scanned between 29+1 and 44 weeks postmenstrual age (PMA) (median 37+1 weeks). Probabilistic tractography of CPC and CTC fibers was performed using constrained spherical deconvolution. Connections between cerebellum and contralateral cerebral hemisphere were identified in all infants studied. Fractional anisotropy (FA) values of CTC and CPC pathways increased with increasing PMA at scan (p < 0.001). The supratentorial regions connecting to contralateral cerebellum in most subjects, irrespective of PMA at scan, included the precentral cortex, superior frontal cortex, supplementary motor area, insula, postcentral cortex, precuneus, and paracentral lobule. This study demonstrates the feasibility of assessing CTC and CPC white matter connectivity in vivo during the early stages of development. The ability to assess cerebellar connectivity during this critical developmental period may help improve our understanding of the role of the cerebellum in a wide range of neuromotor and neurocognitive disorders

The impacts of tumor and tumor associated epilepsy on subcortical brain structures and long distance connectivity in patients with low grade glioma

Low grade gliomas in cerebral cortex often cause symptoms related to higher cerebral functions such as attention, memory and executive function before treatment is initiated. Interestingly, focal tumors residing in one cortical region can lead to a diverse range of symptoms, indicating that the impact of a tumor is extended to multiple brain regions. We hypothesize that the presence of focal glioma in the cerebral cortex leads to alterations of distant subcortical areas and essential white matter tracts. In this study, we analyzed diffusion tensor imaging scans in glioma patients to study the effect of glioma on subcortical gray matter nuclei and long-distance connectivity. We found that the caudate nucleus, putamen and thalamus were affected by cortical glioma, displaying both volumetric and diffusion alterations. The cerebellar cortex contralateral to the tumor side also showed significant volume decrease. Additionally, tractography of the cortico-striatal and cortico-thalamic projections shows similar diffusion alterations. Tumor associated epilepsy might be an important contributing factor to the found alterations. Our findings indeed confirm concurrent structural and connectivity abrasions of brain areas distant from brain tumor, and provide insights into the pathogenesis of diverse neurological symptoms in glioma patients

The Impacts of Tumor and Tumor Associated Epilepsy on Subcortical Brain Structures and Long Distance Connectivity in Patients With Low Grade Glioma

Low grade gliomas in cerebral cortex often cause symptoms related to higher cerebral functions such as attention, memory and executive function before treatment is initiated. Interestingly, focal tumors residing in one cortical region can lead to a diverse range of symptoms, indicating that the impact of a tumor is extended to multiple brain regions. We hypothesize that the presence of focal glioma in the cerebral cortex leads to alterations of distant subcortical areas and essential white matter tracts. In this study, we analyzed diffusion tensor imaging scans in glioma patients to study the effect of glioma on subcortical gray matter nuclei and long-distance connectivity. We found that the caudate nucleus, putamen and thalamus were affected by cortical glioma, displaying both volumetric and diffusion alterations. The cerebellar cortex contralateral to the tumor side also showed significant volume decrease. Additionally, tractography of the cortico-striatal and cortico-thalamic projections shows similar diffusion alterations. Tumor associated epilepsy might be an important contributing factor to the found alterations. Our findings indeed confirm concurrent structural and connectivity abrasions of brain areas distant from brain tumor, and provide insights into the pathogenesis of diverse neurological symptoms in glioma patients

Excellent response to pasireotide therapy in an aggressive and dopamine-resistant prolactinoma.

peer reviewedProlactinomas are the most commonly encountered pituitary adenomas in the clinical setting. While most can be controlled by dopamine agonists, a subset of prolactinomas are dopamine-resistant and very aggressive. In such tumors, the treatment of choice is neurosurgery and radiotherapy, with or without temozolomide. Here, we report a patient with an highly aggressive, dopamine-resistant prolactinoma, who only achieved biochemical and tumor control during pasireotide long-acting release (PAS-LAR) therapy , a second-generation somatostatin receptor ligand (SRL). Interestingly, cystic degeneration, tumor cell necrosis, or both was observed after PAS-LAR administration suggesting an antitumor effect. This case shows that PAS-LAR therapy holds clinical potential in selective aggressive, dopamine-resistant prolactinomas that express somatostatin (SST) receptor subtype 5 and appears to be a potential new treatment option before starting temozolomide. In addition, PAS-LAR therapy may induce cystic degeneration, tumor cell necrosis, or both in prolactinomas