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Year : 2017  |  Volume : 65  |  Issue : 2  |  Page : 253--254

Anaesthesia, chronic pain and brain connectivity

Mary Abraham 
 Department of Anaesthesia, Pain and Palliative Care, Max Hospital, Panchsheel, New Delhi, India

Correspondence Address:
Prof. Mary Abraham
Department of Anaesthesia, Pain and Palliative Care, Max Hospital, Panchsheel, New Delhi - 110 017

How to cite this article:
Abraham M. Anaesthesia, chronic pain and brain connectivity.Neurol India 2017;65:253-254

How to cite this URL:
Abraham M. Anaesthesia, chronic pain and brain connectivity. Neurol India [serial online] 2017 [cited 2023 Feb 1 ];65:253-254
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The advent of functional neuroimaging modalities such as the positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) in the last couple of decades has virtually thrown open a Pandora's box regarding the nuances of brain functioning and connectivity, which were hitherto eluding researchers. These are powerful imaging techniques that can objectively measure subjective behavioral responses and have now become standard tools in neuroscientific research. Both are capable of mapping regional changes in cerebral blood flow and metabolism that occur due to alterations in brain activity, resulting in increased blood flow in areas where neuronal activity increases. But fMRI has several advantages over PET and this has resulted in its widespread use in neuroscientific research, mainly related to unconsciousness, memory and pain perception. Of late, there have been an ever-increasing number of publications using fMRI to understand functional connectivity and neural correlates of consciousness in the brain in physiological as well as pathological states.

Consciousness has been related to the amount of integrated information that the brain is able to generate, and breakdown in brain integration is the neural correlate of the loss of consciousness.[1] These authors stress the important role played by parietal and frontal areas in the generation of consciousness. These functional networks may bind information from endogenous and exogenous sources and make the computational result globally accessible across the brain. Anesthesia may suppress consciousness by disrupting or unbinding this integrative process. Based on animal and human studies, a functional “switch” at the level of the thalamus has been proposed, with inhibition of thalamo-cortical transmission characterizing loss of consciousness.[2]

There is emerging evidence that the behavior of the resting brain under anesthesia and sedation may provide additional important insights into this area rather than the classical concept of observing the neural response to tasks in the awake and sedated patients. Resting state fMRI, which is functional mapping based on spontaneous intrinsic activity, measures spontaneous low frequency fluctuations in blood oxygen level dependent (BOLD) signal and is used to investigate the functional connectivity of the brain during rest. The default mode network (DMN), was one of the first resting networks to be studied and includes the posterior cingulate cortex (PCC), medial prefrontal cortex (MPFC) and bilateral parietal cortices which works maximally under “no task” conditions. The PCC, in particular, has been widely recognized as a major hub in the DMN and is important for consciousness/awareness. In fact, it has been hypothesized that the DMN may be part of a global workspace, a set of cortical neurons whose role is to facilitate exchange of information between remote systems.

The anaesthetic agent propofol, an agonist at the GABA receptor (subtype A), has been used in several studies to evaluate differences in interaction of remote neural networks during altered consciousness. The advantage of using propofol for studying functional connectivity is that it has no major direct effects on cerebrovascular tone and preserves flow-metabolism coupling as compared to other inhalational anaesthetics. Therefore, alterations in BOLD connectivity patterns are more likely to reflect changes in neural activity. Based on the work done by Alkire, it is now thought that propofol acts as tweezers rather than hammers on the brain and its effects on cerebral metabolic rate (CMR) are heterogenous depending on the dose administered.[3] This is in contrast to the hypothesis that anaesthetics act by nonspecific suppression of cerebral metabolism, sometimes called the wet-blanket theory.[4] Boveroux et al., have shown that in healthy adults, propofol-induced unconsciousness is associated with widespread changes in functional connectivity in the human brain, with a preferential targeting in fronto-parietal networks, compared with the relative preservation of early sensory cortices.[5] This suggested a crucial role of higher-order fronto-parietal associative network activity in the genesis of conscious perception.

Patients with chronic pain do not experience just pain, but a host of other disorders as well, such as depression and anxiety, sleep disturbances, and decision making abnormalities and there is evidence that chronic pain could harm cortical areas unrelated to pain. Could this be related to altered functional connectivity in the brain especially in the DMN? And, if so, what is the effect of propofol on resting state functional connectivity in patients with chronic back pain (CBP)?

Chronic back pain has been shown to alter brain dynamics particularly of the DMN,[6] highlighting the impact of enduring pain over brain structure and function. Kregel et al., systematically analyzed the effect of chronic low back pain on the structure and function of the brain using neuroimaging.[7] They found moderate evidence for regional changes in gray and white matter, together with an altered functional connectivity during rest and increased activity in pain-related areas following painful stimulation together with a disrupted DMN. Altered resting state connectivity patterns have been demonstrated in patients with chronic pain associated with fibromyalgia and rheumatoid arthritis.[8] Baliki et al., too found that disruptions of the DMN may underly the cognitive and behavioral impairments accompanying chronic pain.[9]

In this issue, Srinagesh et al., studied resting state brain functional connectivity in an Indian population with chronic back pain receiving propofol sedation.[10] His findings did not differ from what was reported earlier in healthy volunteers under propofol anaesthesia,[11] suggesting that CBP, per se, may not alter the effect of propofol on resting state functional connectivity and that it acts in a similar manner in select areas of the brain as in normal healthy volunteers. The findings of generalized decrease in the integration within large scale brain networks in their study conforms to the known metabolic suppressant effect of propofol with a proportional decrease in cerebral blood flow. Their findings of similar requirements of propofol in patients with chronic pain as compared to healthy volunteers also corroborates with the findings of Bansal et al., who found that propofol requirements were similar in patients with pain due to prolapsed intervertebral discs as compared to patients with brain tumours.[12]

However, considering the fact that there is altered structural and functional connectivity in patients with chronic low back pain,[7] further research is needed to confirm the findings of Srinagesh et al., and to clarify the relationship between chronic pain, neuroplastic changes and the requirement of anaesthetics in these patients using functional neuroimaging.


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