Deans' stroke musings: Alterations of Functional Connectivity in Stroke Patients With Basal Ganglia Damage and Cognitive Impairment

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Saturday, September 19, 2020

Alterations of Functional Connectivity in Stroke Patients With Basal Ganglia Damage and Cognitive Impairment

You have described a problem but DONE NOTHING TO SOLVE IT. Useless.

Alterations of Functional Connectivity in Stroke Patients With Basal Ganglia Damage and Cognitive Impairment

Guanqun Yao¹^†,

Jing Li^1,2^†,

Sha Liu^1,2,

Jiaojian Wang^3,4,

Xiaohua Cao¹,

Xinrong Li¹,

Long Cheng¹,

Huafu Chen³ and

Yong Xu^1,2,5^*

¹Department of Psychiatry, First Hospital/First Clinical Medical College of Shanxi Medical University, Taiyuan, China
²Shanxi Key Laboratory of Artificial Intelligence Assisted Diagnosis and Treatment for Mental Disorder, First Hospital of Shanxi Medical University, Taiyuan, China
³The Clinical Hospital of Chengdu Brain Science Institute, MOE Key Lab for Neuroinformation, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, China
⁴Center for Language and Brain, Shenzhen Institute of Neuroscience, Shenzhen, China
⁵MDT Center for Cognitive Impairment and Sleep Disorders, First Hospital of Shanxi Medical University, Taiyuan, China

Background: Stroke with basal ganglia damage (SBG) is a neurological disorder characterized by cognitive impairment. The neurobiological mechanism of cognitive impairment in stroke patients with basal ganglia damage (SBG patients) remains unclear. This study aimed to explore the underlying neurobiological mechanism of cognitive impairment in SBG patients using resting-state functional magnetic resonance imaging (rs-fMRI).

Methods: The differences in functional connectivity (FC) between 14 SBG patients (average age: 61.00 ± 7.45 years) and 21 healthy controls (HC) (average age: 60.67 ± 6.95 years) were examined using voxel-mirrored homotopic connectivity (VMHC) and degree centrality (DC). Moreover, we compared the cognitive functions of SBG patients with HC using the Chinese Revised Wechsler Adult Intelligence Scale (WAIS-RC) and Wechsler Memory Scale (WMS).

Results: Full-scale intelligence quotient (FIQ) (t = 2.810, p < 0.010) and memory quotient (MQ) (t = 2.920, p < 0.010) scores of SBG patients were significantly lower than those of HC. Compared with HC, significantly decreased VMHC values in the bilateral angular gyrus, supramarginal gyrus, inferior frontal gyrus, middle temporal gyrus, hippocampus, precuneus, precentral gyrus, and middle occipital gyrus and decreased DC values in the right supramarginal gyrus, bilateral angular gyrus, and right postcentral gyrus were observed in SBG patients. Moreover, the VMHC values in the angular gyrus, inferior frontal gyrus, supramarginal gyrus, and middle temporal gyrus and the DC values in the right supramarginal gyrus were significantly correlated with cognitive functions in all participants.

Conclusion: Our findings may provide a neural basis for cognitive impairments in SBG patients. Furthermore, local abnormalities of functional networks and interhemispheric interaction deficits may provide new ideas and insights for understanding and treating SBG patients' cognitive impairments.