Posts tagged anesthesia
Articles and news from the latest research reports.
Common Brain Processes of Anesthetic-Induced Unconsciousness Identified
A study from the June issue of Anesthesiology found feedback from the front region of the brain is a crucial building block for consciousness and that its disruption is associated with unconsciousness when the anesthetics ketamine, propofol or sevoflurane are administered.
Brain centers and mechanisms of consciousness have not been well understood, resulting in a need for better monitors of consciousness during anesthesia. In addition, how anesthetics with different structures and pharmacological properties can generate unconsciousness has been a persistent question in anesthesiology since the beginning of the field in the mid-19th century.
A team of researchers from the University of Michigan, Ann Arbor, Mich., and Asan Medical Center, Seoul, South Korea, conducted a brain wave (electroencephalographic, or EEG) study of the front and back regions of the brain in 30 surgical patients who received intravenous ketamine. They compared the results of this study to the EEG data collected from 18 surgical patients who received either intravenous propofol or inhaled sevoflurane in a previous study. These three anesthetics, known to act on different parts of the brain and produce different EEG patterns, had the same effect of disrupting communication in the brain.
“Understanding a commonality among the actions of these diverse drugs could lead to a more comprehensive theory of how general anesthetics induce unconsciousness,” said study author George Mashour, M.D., Ph.D., assistant professor and associate chair for faculty affairs, Department of Anesthesiology, University of Michigan. “Our research shows that studying general anesthesia from the perspective of consciousness may be a fruitful approach and create new avenues for further investigation of anesthetic mechanisms and monitoring.”
An accompanying editorial by Jamie W. Sleigh, M.D., professor of anaesthesiology and intensive care, Department of Anaesthesia, University of Auckland, Hamilton, New Zealand, supported the study’s ability to better understand the neurobiology of consciousness.
“If the study’s findings are confirmed by subsequent work, the paper will achieve landmark status,” said Dr. Sleigh. “The study not only sheds light on the phenomenon of general anesthesia, but also how it is necessary for certain regions of the brain to communicate accurately with one another for consciousness to emerge.”
In addition, Dr. Sleigh recognized the study’s potential to lead to the development of better depth-of-anesthesia monitors that work for all general anesthetics.
(Image: Shutterstock)
Anesthetic Linked to Brain Cell Death in Newborn Mice
Exposure to the anesthetic agent isoflurane increases “programmed cell death” of specific types of cells in the newborn mouse brain, reports a study in the April issue of Anesthesia & Analgesia, official journal of the International Anesthesia Research Society (IARS).
With prolonged exposure, a common inhaled anesthesia eliminates approximately two percent of neurons in the cortex of newborn mice. Although its relevance to anesthesia in human newborns remains to be determined, the study by Dr George K. Istaphanous and colleagues of Cincinnati Children’s Hospital Medical Center provides unprecedented detail on the cellular-level effects of anesthetics on the developing brain.
Isoflurane Exposure Increases ‘Programmed Death’ of Brain Cells
In the study, seven-day-old mice were exposed to isoflurane for several hours. After exposure, sophisticated examinations were performed to assess the extent of isoflurane-induced brain cell death, including the specific types, locations, and functions of brain cells lost.
Isoflurane exposure led to widespread increases programmed cell death, called apoptosis, throughout the brain. Although cell loss was substantially higher after isoflurane exposure, the cell types lost were similar to the cells lost in the apoptosis that is part of normal brain maturation. In both cases, mainly neurons were lost. Neurons are the cells that transmit and store information.
The rate of cell death in the superficial cortex—the thick outer layer of the brain—was at least eleven times higher in isoflurane-exposed animals than seen with normal brain maturation. Overall, approximately two percent of cortical neurons were lost after isoflurane exposure. Astrocytes, another major type of cortical brain cells, were less affected by anesthetic exposure.
Relevance to Anesthesia in Human Newborns Is Unclear—For Now
A growing body of evidence suggests that isoflurane and similar anesthetics may have toxic effects on brain cells in newborn animals and humans. “However, neither the identity of dying cortical cells nor the extent of cortical cell loss has been sufficiently characterized,” according to Dr Istaphanous and colleagues.
The new study provides detailed information on the extent and types of brain cell loss resulting from prolonged isoflurane exposure in newborn mice. It’s unclear whether the two percent brain cell loss induced in the experiments would lead to any permanent damage—in previous studies, newborn isoflurane-exposed mice showed no obvious brain damage long after the exposure.
It can’t be assumed that isoflurane causes similar patterns of cellular damage in human newborns requiring general anesthesia, Dr Istaphanous and coauthors emphasize. Some studies have linked early-life exposure to anesthesia and surgery to later behavioral and learning abnormalities. Other studies have found no adverse affects on children exposed to anesthetics during vulnerable times of brain development. Further research on the selective nature and molecular mechanisms of isoflurane-induced brain cell death would be needed to determine the relevance of the experimental findings, if any, to human infants undergoing anesthesia.
(Source: newswise.com)
How the brain loses and regains consciousness
Study reveals brain patterns produced by a general anesthesia drug; work could help doctors better monitor patients.
Since the mid-1800s, doctors have used drugs to induce general anesthesia in patients undergoing surgery. Despite their widespread use, little is known about how these drugs create such a profound loss of consciousness.
In a new study that tracked brain activity in human volunteers over a two-hour period as they lost and regained consciousness, researchers from MIT and Massachusetts General Hospital (MGH) have identified distinctive brain patterns associated with different stages of general anesthesia. The findings shed light on how one commonly used anesthesia drug exerts its effects, and could help doctors better monitor patients during surgery and prevent rare cases of patients waking up during operations.
Anesthesiologists now rely on a monitoring system that takes electroencephalogram (EEG) information and combines it into a single number between zero and 100. However, that index actually obscures the information that would be most useful, according to the authors of the new study, which appears in the Proceedings of the National Academy of Sciences the week of March 4.
“When anesthesiologists are taking care of someone in the operating room, they can use the information in this article to make sure that someone is unconscious, and they can have a specific idea of when the person may be regaining consciousness,” says senior author Emery Brown, an MIT professor of brain and cognitive sciences and health sciences and technology and an anesthesiologist at MGH.
Rapid fragmentation of neuronal networks at the onset of propofol-induced unconsciousness
General anesthesia involves rapidly inducing a reversible coma by administering a large dose of a fast-acting drug, such as propofol. Previous research has demonstrated that propofol enhances inhibitory input to neurons throughout the spinal cord, brainstem, thalamus, and cortex. However, how these effects in single cells translate to larger-scale neural circuits and cause unconsciousness is not well understood. We recorded spiking activity from ensembles of single neurons and intracranial electrical activity during the induction of propofol general anesthesia in human subjects undergoing surgery. We found that loss of consciousness (LOC) corresponds to the abrupt onset of a slow cortical oscillation that marks a fragmentation of neuronal networks. These results identify the slow oscillation as a dramatic neural correlate of LOC and demonstrate that slow oscillation marks the transition into a brain state in which local neuronal networks are isolated, impairing both temporal and spatial communication throughout the cortex.
Inside the unconscious brain
A new study from MIT and Massachusetts General Hospital (MGH) reveals, for the first time, what happens inside the brain as patients lose consciousness during anesthesia.
By monitoring brain activity as patients were given a common anesthetic, the researchers were able to identify a distinctive brain activity pattern that marked the loss of consciousness. This pattern, characterized by very slow oscillation, corresponds to a breakdown of communication between different brain regions, each of which experiences short bursts of activity interrupted by longer silences.
“Within a small area, things can look pretty normal, but because of this periodic silencing, everything gets interrupted every few hundred milliseconds, and that prevents any communication,” says Laura Lewis, a graduate student in MIT’s Department of Brain and Cognitive Sciences (BCS) and one of the lead authors of a paper describing the findings in the Proceedings of the National Academy of Sciences this week.
This pattern may help anesthesiologists to better monitor patients as they receive anesthesia, preventing rare cases where patients awaken during surgery or stop breathing after excessive doses of anesthesia drugs.
A syndrome called “post-operative cognitive decline” has been coined to refer to the commonly reported loss of cognitive abilities, usually in older adults, in the days to weeks after surgery. In fact, some patients time the onset of their Alzheimer’s disease symptoms from a surgical procedure. Exactly how the trio of anesthesia, surgery, and dementia interact is clinically inconclusive, yet of great concern to patients, their families and physicians.
A year ago, researchers at the Perelman School of Medicine at the University of Pennsylvania reported that Alzheimer’s pathology, as reflected by cerebral spinal fluid biomarkers, might be increased in patients after surgery and anesthesia. However, it is not clear whether the anesthetic drugs or the surgical procedure itself was responsible. To separate these possibilities, the group turned to a mouse model of Alzheimer’s disease.
The results, published online this month in the Annals of Surgery, show that surgery itself, rather than anesthesia, has the more profound impact on a dementia-vulnerable brain.