scholarly journals Quantitative Changes in Regional Cerebral Blood Flow Induced by Cold, Heat and Ischemic Pain

2012 ◽  
Vol 117 (4) ◽  
pp. 857-867 ◽  
Author(s):  
Michael A. Frölich ◽  
Hrishikesh Deshpande ◽  
Timothy Ness ◽  
Georg Deutsch

Background The development of arterial spin labeling methods has allowed measuring regional cerebral blood flow (rCBF) quantitatively and to show the pattern of cerebral activity associated with any state such as a sustained pain state or changes due to a neurotropic drug. Methods The authors studied the differential effects of three pain conditions in 10 healthy subjects on a 3 Tesla scanner during resting baseline, heat, cold, and ischemic pain using continuous arterial spin labeling. Results Cold pain showed the greatest absolute rCBF increases in left anterior cingulate cortex, left amygdala, left angular gyrus, and Brodmann area 6, and a significant rCBF decrease in the cerebellum. Changes in rCBF were characteristic of the type of pain condition: cold and heat pain showed increases, whereas the ischemic condition showed a reduction in mean absolute gray matter flow compared with rest. An association of subjects' pain tolerance and cerebral blood flow was noted. Conclusions The observation that quantitative rCBF changes are characteristic of the pain task used and that there is a consistent rCBF change in Brodman area 6, an area responsible for the integration of a motor response to pain, should provide extremely useful information in the quest to develop an imaging biomarker of pain. Conceivably, response in BA6 may serve as an objective measure of analgesic efficacy.

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S142-S142
Author(s):  
Kamiyu Ogyu ◽  
Shiori Honda ◽  
Karin Matsushita ◽  
Yoshihiro Noda ◽  
Hideo Kato ◽  
...  

Abstract Background Approximately 30% of patients with schizophrenia do not respond to antipsychotics, which is called treatment-resistant schizophrenia (TRS). A recent systematic review showed decreased regional cerebral blood flow (rCBF) in the cerebral cortex and increased rCBF in the putamen in patients with schizophrenia. However, to date, no study has examined rCBF using arterial spin labeling (ASL) in patients with TRS. Thus, we compared rCBF between patients with TRS and those with non-TRS to investigate neural basis of this condition. Methods We acquired whole-brain rCBF measurements using 1.5T magnetic resonance imaging (MRI) with pseudo-continuous ASL in those with TRS and non-TRS. TRS was defined as 1) a Clinical Global Impression Severity (CGI-S) score of ≧ 4 (moderate) and 2) a score of ≧ 4 (moderate) on two Positive and Negative Syndrome Scale (PANSS) positive symptom items after optimal antipsychotic treatment. Non-TRS was defined as 1) a CGI-S score of ≦3, 2) scores of ≦ 3 on all positive symptom items of the PANSS, and 3) no symptomatic relapse during the previous 3 months. Optimal antipsychotic treatment was defined as ≧ 6 consecutive weeks with ≧ 400 mg of chlorpromazine (CPZ) equivalent daily dose antipsychotic treatment. The rCBF maps were subsequently derived from the proton-density-weighted reference images. Group differences in rCBF between the two groups (non-TRS vs. TRS) were tested using two sample t-test with age, gender, and PANSS positive scores as covariates. Multiple comparisons were corrected using familywise error (FWE) method with a significance threshold of P <.05. Results A total of 32 participants were included (13 TRS [6 females, age= 41.2±9.8, PANSS=80.3±9.7] and 19 non-TRS [6 females, age= 40.6±11.9, PANSS=58.9±10.0]). rCBF in the cerebellum was increased in the TRS group compared with the non-TRS group. In addition, there are inverse correlation between rCBF in the cerebellum and PANSS positive score in the non-TRS group. Discussion These preliminary results suggest that perfusion in the cerebellum may be implicated in the pathophysiology of TRS. This study will continue to enroll participants (our target sample is 30/each group). To identify the abnormal rCBF in patients with TRS will facilitate elucidating the pathophysiology of TRS and pave a way of developing novel treatment of this difficult-to-treat population.


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