Step-down vs. step-up noxious stimulation: differential effects on pain perception and patterns of brain activation

2015 ◽  
Vol 60 (1) ◽  
pp. 117-127 ◽  
Author(s):  
J. C. Choi ◽  
J. Kim ◽  
E. Kang ◽  
J.-H. Choi ◽  
W. Y. Park ◽  
...  
Keyword(s):  
Pain Perception ◽  
Brain Activation ◽  
Noxious Stimulation ◽  
Differential Effects ◽  
Step Down

scholarly journals Pharmacologic Modulation of Noxious Stimulus-evoked Brain Activation in Cynomolgus Macaques Observed with Functional Neuroimaging

2020 ◽  
Vol 59 (1) ◽  
pp. 94-103
Author(s):  
Tomomi Shirai ◽  
Mizuho Yano ◽  
Takahiro Natsume ◽  
YūJi Awaga ◽  
Yoshitaka Itani ◽  
...  
Keyword(s):  
Pain Perception ◽  
Functional Neuroimaging ◽  
Analgesic Efficacy ◽  
Insular Cortex ◽  
Brain Activation ◽  
Noxious Stimulation ◽  
Invasive Procedures ◽  
Apparent Lack ◽  
Cynomolgus Macaques ◽  
The Brain

Maintaining effective analgesia during invasive procedures performed under general anesthesia is important for minimizing postoperative complications and ensuring satisfactory patient wellbeing and recovery. While patients under deep sedation may demonstrate an apparent lack of response to noxious stimulation, areas of the brain related to pain perception may still be activated. Thus, these patients may still experience pain during invasive procedures. The current study used anesthetized or sedated cynomolgus macaques and functional magnetic resonance imaging (fMRI) to assess the activation of the parts of the brain involved in pain perception during the application of peripheral noxious stimuli. Noxious pressure applied to the foot resulted in the bilateral activation of secondary somatosensory cortex (SII) and insular cortex (Ins), which are both involved in pain perception, in macaques under either propofol or pentobarbital sedation. No activation of SII/Ins was observed in macaques treated with either isoflurane or a combination of medetomidine, midazolam, and butorphanol. No movement or other reflexes were observed in response to noxious pressure during stimulation under anesthesia or sedation. The current findings show that despite the lack of visible behavioral symptoms of pain during anesthesia or sedation, brain activation suggests the presence of pain depending on the anesthetic agent used. These data suggest that fMRI could be used to noninvasively assess pain and to confirm the analgesic efficacy of currently used anesthetics. By assessing analgesic efficacy, researchers may refine their experiments, and design protocols that improve analgesia under anesthesia.

Differential effects of eyes open or closed in darkness on brain activation patterns in blind subjects

2009 ◽  
Vol 466 (1) ◽  
pp. 30-34 ◽  
Author(s):  
K. Hüfner ◽  
T. Stephan ◽  
V.L. Flanagin ◽  
A. Deutschländer ◽  
A. Stein ◽  
...  
Keyword(s):  
Brain Activation ◽  
Activation Patterns ◽  
Differential Effects ◽  
Eyes Open

Supraspinal Anesthesia

2006 ◽  
Vol 105 (4) ◽  
pp. 764-778 ◽  
Author(s):  
Izabela Jugovac ◽  
Olga Imas ◽  
Anthony G. Hudetz
Keyword(s):  
Spinal Cord ◽  
Pain Perception ◽  
Drug Distribution ◽  
Noxious Stimulation ◽  
Tail Pinch ◽  
Delta Power ◽  
Intracerebroventricular Infusion ◽  
Power Increase ◽  
Beta Power ◽  
Gamma Power

Background Anesthetic endpoints of unconsciousness and immobility result from agent effects on both brain and spinal cord that are difficult to separate during systemic administration. To investigate cerebral mechanism of anesthetic-induced unconsciousness, the authors studied behavioral and electrophysiologic effects of four anesthetics infused intracerebroventricularly to conscious rats. The authors aimed to produce progressively increasing anesthetic depths, indicated by electro-encephalographic synchronization and behavioral change. Methods During anesthesia, rats were equipped with intracerebroventricular infusion catheters, hind-paw stimulation, and epidural electrodes to record the electroencephalogram from the somatosensory cortex. Silicone bolus was injected into the fourth ventricle to minimize drug distribution to the spinal cord. 60 min later, 50-min infusion of pentobarbital (6.0 mg/h), fentanyl (0.75 microg/h), propofol (3.0 mg/h), or midazolam (0.24 mg/h) was initiated. Vibrissal, olfactory, corneal, and tail-pinch responses were tested every 10 min. Results All agents depressed vibrissal, olfactory, and corneal responses; propofol and pentobarbital produced the strongest effect. All agents except propofol depressed tail-pinch response; fentanyl and pentobarbital produced the strongest effect. All agents except midazolam increased delta power. Pentobarbital enhanced theta power. All agents except fentanyl enhanced alpha and beta power. Pentobarbital and midazolam slightly increased, whereas fentanyl decreased, gamma power. Pentobarbital increased and midazolam decreased somatosensory evoked potential; these changes were small and apparently unrelated to behavior. Conclusions Alpha and beta power increase may reflect sedative component of anesthesia. Simultaneous delta, alpha, and beta power increase may correlate with loss of consciousness. Theta and delta power increase may reflect surgical anesthesia. Opioid-induced gamma power decrease may reflect suppression of pain perception. Pentobarbital-, fentanyl-, and midazolam-induced immobility to noxious stimulation may be mediated supraspinally.

scholarly journals Neural Plasticity in Common Forms of Chronic Headaches

2015 ◽  
Vol 2015 ◽  
pp. 1-14 ◽  
Author(s):  
Tzu-Hsien Lai ◽  
Ekaterina Protsenko ◽  
Yu-Chen Cheng ◽  
Marco L. Loggia ◽  
Gianluca Coppola ◽  
...  
Keyword(s):  
Neural Plasticity ◽  
Pain Perception ◽  
Medication Overuse Headache ◽  
Tension Type Headache ◽  
Pain Modulation ◽  
Noxious Stimulation ◽  
Acute Setting ◽  
Pain Chronification ◽  
Chronic Headaches ◽  
Type Headache

Headaches are universal experiences and among the most common disorders. While headache may be physiological in the acute setting, it can become a pathological and persistent condition. The mechanisms underlying the transition from episodic to chronic pain have been the subject of intense study. Using physiological and imaging methods, researchers have identified a number of different forms of neural plasticity associated with migraine and other headaches, including peripheral and central sensitization, and alterations in the endogenous mechanisms of pain modulation. While these changes have been proposed to contribute to headache and pain chronification, some findings are likely the results of repetitive noxious stimulation, such as atrophy of brain areas involved in pain perception and modulation. In this review, we provide a narrative overview of recent advances on the neuroimaging, electrophysiological and genetic aspects of neural plasticity associated with the most common forms of chronic headaches, including migraine, cluster headache, tension-type headache, and medication overuse headache.

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