scholarly journals Dynamic Brain Activity Following Auricular Point Acupressure in Chemotherapy-Induced Neuropathy: A Pilot Longitudinal Functional Magnetic Resonance Imaging Study

2020 ◽  
Vol 9 ◽  
pp. 216495612090609
Author(s):  
Chao Hsing Yeh ◽  
Keenan Caswell ◽  
Sonaali Pandiri ◽  
Haris Sair ◽  
Nada Lukkahatai ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Functional Magnetic Resonance Imaging ◽  
Brain Activity ◽  
Pilot Trial ◽  
Anterior Cingulate ◽  
Functional Magnetic Resonance ◽  
Resonance Imaging ◽  
Delayed Imaging ◽  
Auricular Point

Background The objective of this study was to investigate the dynamic brain activity following auricular point acupressure (APA) in chemotherapy-induced neuropathy (CIN). Methods Participants received 4 weeks of APA in an open-pilot trial with repeated observation. Along with the clinical self-reported CIN outcomes, objective outcomes were measured over the course of the treatment by physiological changes in pain sensory thresholds from quantitative sensory testing (QST) and repeated functional magnetic resonance imaging scans. Results After 4 weeks of APA, participants had reported clinically significant improvements (ie, ≥30%) in a reduction of CIN symptoms (including pain, numbness, tingling, and stiffness) in lower extremity stiffness (32%), reduced foot sensitivity (13%), and higher pain threshold (13%). Across the 11 intrinsic brain networks examined, there was a trend toward significance of the connectivity of the basal ganglia network (BGN) to the salience network (SAL), which was decreased pre-APA versus immediate-APA (effect size [ES] = 1.04, P = .07). The BGN also demonstrated decreased connectivity with the language network pre-APA versus delayed imaging post-APA (ES = −0.92, P = .07). Furthermore, there was increased executive control network (ECN) and SAL within-network connectivity comparing pre-APA to delayed imaging post-APA, trending toward significance (ES = 0.41, P = .09 and ES = 0.17, P = .09, respectively). Conclusion The changes in connectivity and activity within or between the ECN, SAL, and BGN from pre- to post-APA suggest ongoing alterations in brain functional connectivity following APA, particularly in the insula, anterior cingulate, and dorsolateral prefrontal cortices, which play significant roles in pain, memory, and cognitive function.

Examination of processing speed deficits in multiple sclerosis using functional magnetic resonance imaging

2009 ◽  
Vol 15 (3) ◽  
pp. 383-393 ◽  
Author(s):  
HELEN M. GENOVA ◽  
FRANK G. HILLARY ◽  
GLENN WYLIE ◽  
BART RYPMA ◽  
JOHN DELUCA
Keyword(s):  
Magnetic Resonance Imaging ◽  
Multiple Sclerosis ◽  
Magnetic Resonance ◽  
Functional Magnetic Resonance Imaging ◽  
Processing Speed ◽  
Anterior Cingulate ◽  
Precentral Gyrus ◽  
Functional Magnetic Resonance ◽  
Resonance Imaging ◽  
Group Processing

AbstractAlthough it is known that processing speed deficits are one of the primary cognitive impairments in multiple sclerosis (MS), the underlying neural mechanisms responsible for impaired processing speed remain undetermined. Using BOLD functional magnetic resonance imaging, the current study compared the brain activity of 16 individuals with MS to 17 healthy controls (HCs) during performance of a processing speed task, a modified version of the Symbol Digit Modalities Task. Although there were no differences in performance accuracy, the MS group was significantly slower than HCs. Although both groups showed similar activation involving the precentral gyrus and occipital cortex, the MS showed significantly less cerebral activity than HCs in bilateral frontal and parietal regions, similar to what has been reported in aging samples during speeded tasks. In the HC group, processing speed was mediated by frontal and parietal regions, as well as the cerebellum and thalamus. In the MS group, processing speed was mediated by insula, thalamus and anterior cingulate. It therefore appears that neural networks involved in processing speed differ between MS and HCs, and our findings are similar to what has been reported in aging, where damage to both white and gray matter is linked to processing speed impairments (JINS, 2009, 15, 383–393).

scholarly journals Effect of Subanesthetic Ketamine on Intrinsic Functional Brain Connectivity

2012 ◽  
Vol 117 (4) ◽  
pp. 868-877 ◽  
Author(s):  
Marieke Niesters ◽  
Najmeh Khalili-Mahani ◽  
Christian Martini ◽  
Leon Aarts ◽  
Joop van Gerven ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Functional Magnetic Resonance Imaging ◽  
Anterior Cingulate Cortex ◽  
Resting State ◽  
Brain Connectivity ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Functional Magnetic Resonance ◽  
Resonance Imaging

Background The influence of psychoactive drugs on the central nervous system has been investigated with positron emission tomography and task-related functional magnetic resonance imaging. However, it is not known how these drugs affect the intrinsic large-scale interactions of the brain (resting-state functional magnetic resonance imaging connectivity). In this study, the effect of low-dose S(+)-ketamine on intrinsic brain connectivity was investigated. Methods Twelve healthy, male volunteers received a 2-h intravenous S(+)-ketamine infusion (first hour 20 mg/70 kg, second hour 40 mg/70 kg). Before, during, and after S(+)-ketamine administration, resting-state brain connectivity was measured. In addition, heat pain tests were performed between imaging sessions to determine ketamine-induced analgesia. A mixed-effects general linear model was used to determine drug and pain effects on resting-state brain connectivity. Results Ketamine increased the connectivity most importantly in the cerebellum and visual cortex in relation to the medial visual network. A decrease in connectivity was observed in the auditory and somatosensory network in relation to regions responsible for pain sensing and the affective processing of pain, which included the amygdala, insula, and anterior cingulate cortex. Connectivity variations related to fluctuations in pain scores were observed in the anterior cingulate cortex, insula, orbitofrontal cortex, and the brainstem, regions involved in descending inhibition of pain. Conclusions Changes in connectivity were observed in the areas that explain ketamine's pharmacodynamic profile with respect to analgesia and psychedelic and other side effects. In addition, pain and ketamine changed brain connectivity in areas involved in endogenous pain modulation.

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