Why does versed cause amnesia

This study could not demonstrate any measurable degree of retrograde amnesia for visual or event memory with i. We did identify the ability of i. However, there was a significant difference in the recall of events at the time of midazolam administration with higher doses of midazolam 5 and 10 mg resulting in a lower recall rate of the current event, mask preoxygenation.

This event was timed to occur simultaneously with the administration of midazolam, but continued until induction of anaesthesia.

Given that this occurred before a meaningful effect site concentration of midazolam could have been achieved, it suggests a possibility of immediate retrograde amnesia. However, if such an effect exists, it must truly be near-instantaneous as it does not affect memory of events in the minutes before midazolam administration. Almost all patients were able to recollect events at 1, 2 and 4 min prior to midazolam administration.

In our study we chose to include the time period immediately prior to the administration of the drug, which is a time period not tested in the literature to date and, indeed, the time period most likely to be useful if any degree of retrograde amnesia was to be found.

Our study also confirmed that the level of sedation, as measured by BIS and VAS, increases following administration of midazolam in a dose-dependent manner. This finding, although not new, illustrates a strong point of our study design in that we achieved effective sedation levels typical of routine practice.

The extent of sedation as measured by BIS was correlated with anterograde amnesia as measured by event recall. Sedation will affect consciousness of current events and can be expected to impair memory processing. The increased amnesia demonstrated in the time period after study drug administration was closer to the time of induction when propofol was administered.

It should also be recognized that midazolam administration during anaesthesia may be influenced by amnesic effects of propofol or other coadministered hypnotic drugs.

More than 20 different tests have been reported in the literature for measuring an amnesic effect of midazolam. This indicates a lack of spurious reporting and supports the reliability of the memory-testing procedures.

A few patients in the control group could not recall some events or posters, which illustrates that some of the measured amnesia could be due to inattention or inability to retrieve memory; this can be attributed to the study environment in the operating theatre, immediately before induction of anaesthesia.

Naturally these factors affect all patients and it highlights the importance of including a control group in such research. We studied 10 participants in each group; it remains possible that we could have missed a small effect of midazolam-induced retrograde amnesia, but we believe that if such an effect exists, it would have little, if any, clinical utility. Our study sample size calculation was partly guided by previous studies but, because each had used different methodologies, the final estimates were based on what we considered to be a clinically important difference.

We chose to analyse the midazolam dose effect using general linear models, but such an approach did not allow us to estimate study power accurately. Our study did not take into consideration all types of memory, as it would have been impractical to perform all the necessary tests simultaneously. In particular, it is important to differentiate explicit recall from implicit recall detected by special testing, and to differentiate recognition memory from other sensory modalities hearing, touch and olfaction.

We did not include a test of auditory memory, which would be particularly useful in the context of awareness prevention during surgery, since heard voices and sounds are commonly involved in awareness reports. It is a common belief that the amnesic properties of midazolam can be used to prevent or treat suspected awareness. Immediate anterograde amnesia can be achieved, and this may be of some clinical utility in reducing the risk of awareness at specific times during surgery.

We found that i. However, i. This may be useful in preventing explicit recall of perioperative events. Effects of diazepam and scopolamine on storage, retrieval and organizational processes in memory. Psychopharmacologia ; 44 : — Diazepam and memory: support for a duplex model of memory.

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Pharmacodynamic modeling of the electroencephalographic effects of midazolam and diazepam. Despite common neural changes related to anesthesia, there are some specific effects on brain function for other anesthetic drugs. Numerous studies have suggested that anesthetic-induced sedation disturbs cerebral connectivity.

However, the drug effects on higher-order brain networks still vary among diverse anesthetic agents [ 6 ]. For example, in our previous work, no significant functional connectivity changes within the DMN were observed during midazolam-induced light sedation [ 66 ].

In contrast, significant reductions in resting-state functional connectivity for DMN were reported during propofol or ketamine-induced mild sedation [ 78 , 88 , 89 ]. Midazolam or propofol-induced decrease in consciousness correlates with decreased functional connectivity within the FPN, whereas ketamine administration leads to no significant reduction in the connectivity strength in the FPN [ 66 , 88 , 89 ].

For the salience network, midazolam-induced sedation barely affects it, whereas the strongest effect of ketamine administration is observed in the salience network [ 66 , 78 ].

On the other hand, the previous studies are consistent with the notion that auditory network is minimally affected during midazolam or propofol-induced sedation [ 66 , 88 ].

However, ketamine administration significantly decreases functional connectivity with auditory network [ 78 , ].

Compared with studies using midazolam, thalamocortical system, which is a bilateral structure and has two thalamic nuclei, the specific and nonspecific divisions, are involved in propofol-induced anesthesia [ , , ]. The specific thalamocortical network, which contains dominantly medial and bilateral frontal and temporal areas, is moderately affected, while the nonspecific thalamocortical network, which contains medial frontal and medial parietal areas, is severely suppressed during propofol-induced sedation [ ].

These findings have not yet been observed in studies related to midazolam. For decades, anesthetic agents are used to manipulate the global level of consciousness to explore the neural correlates of consciousness in healthy individuals. Combined with various neuroimaging techniques, the studies are consistent with the notion that the cortex and subcortical structures are suppressed sequentially in a dose-dependent manner [ 6 ].

Broadly speaking, depending on the anesthetic agent and dose, it may produce different levels and contents of consciousness described as a scale ranging from vivid wakefulness, to light sedation, to deep sedation, final to total unconsciousness [ 84 , ].

The level of consciousness sometimes represents the degree of arousal which can be assessed by purposeful response to verbal command. The content of consciousness is sometimes used synonymously with awareness which can be determined by cognitive testing [ 85 ].

Based on recent literature, the consciousness can be divided into three different states including a state of connected consciousness awareness of the environment , a state of disconnected consciousness only awareness of self and unconsciousness a complete absence of subjective experience along with increased anesthetic concentration [ 85 , ].

Currently, most studies with midazolam still focus on a certain state of consciousness. Coupled with multimodal neuroimaging which combines data obtained from multiple neuroimaging techniques, future work in a larger sample size including participants who have submitted to stepwise increments in anesthetic agent concentration, up to unconsciousness is expected to enable a comprehensive and accurate understanding of neural substrates of consciousness.

There is growing evidence that functional brain dynamics captures important information about cognition and the emergence of momentary neural coalitions forms the basis for complex cognitive functions, such as consciousness [ , ]. Like many other complex systems, the brain exhibits a wide range of dynamic activity and connectivity patterns that are thought to be fundamental for processing information in the course of cognition [ , , ]. However, to date, most of the fMRI research has focused on changes in static functional connectivity patterns during midazolam-induced light sedation [ 66 , 69 ].

A systematic analysis of changes in temporal and spatial properties of dynamic connectivity networks during midazolam-induced alteration of consciousness is an area for future work. Moreover, functional connectivity describes the statistical dependencies between two or more variables and does not provide information about the directed casual interactions among brain regions [ , , ].

Furthermore, functional connectivity analyses make minimal assumptions about the physical mechanisms and may not reflect correlations among neuronal activity. These limitations call for an approach in terms of effective connectivity [ ]. Effective connectivity refers causal influence that one neural system exerts over another, either at a synaptic or a population level [ ].

The related follow-up studies are expected to identify dynamic effective connectivity changes during midazolam-induced alteration of consciousness for better understanding the detailed circuitry underlying consciousness. In addition, previous studies suggested that anesthetic agent can indirectly affect BOLD signaling by altering physiological parameters, such as arterial concentration of carbon dioxide.

Since individuals are not intubated but spontaneously ventilate during midazolam-induced sedation, respiratory depression associated with intravenous midazolam may have resulted in hypercapnia and increased arterial CO 2 levels [ ].

During this condition, certain regions of gray matter appeared to have greater cerebrovascular responses to changes in the partial pressure of carbon dioxide PaCO 2 and partial pressure of oxygen PaO 2 than did others [ ]. In this review, we have summarized neuroimaging mechanisms of midazolam-induced sedation or anesthesia, which is important for understanding how midazolam-induced sedation impacts on various domains of cognition and the patterns of preserved brain activity during sedation.

Studies of individuals who are sedated with midazolam suggest that cortical activity is sequentially impaired from higher-order brain cortices to primary cortical areas in a dose-dependent manner. Under midazolam-induced sedation, functional connectivity within lower-level networks is preserved.

By contrast, functional connectivity within and between higher-order networks, particularly the anticorrelation between the DAN and the DMN, is seemingly of neuronal origin of consciousness.

Nevertheless, although much published work has suggested the effective role of preserved brain activity in the emergence of the conscious awareness, more evidence should still be required to further explore brain mechanisms of midazolam-induced alteration of consciousness.

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Versed can cause respiratory depression, meaning the urge to breathe is decreased. Due to this side effect, you should be closely monitored in a healthcare facility while on Versed. Versed can also increase the respiratory depression effects of other medications, including opioids. Due to this respiratory depression effect, patients with respiratory conditions such as COPD may not be good candidates for Versed.

People on a ventilator, who may or may not have a respiratory disease, may be given Versed to help them tolerate having a breathing tube in place. Versed can decrease blood pressure and should be used with caution when a patient has low blood pressure, whether it is caused by shock, sepsis or a normal state for the patient.

Versed should be used with caution in anyone who's breastfeeding or pregnant. It's been shown to cross the placental barrier, meaning that the fetus will receive some of the drug. Versed is excreted more slowly in people with diminished kidney function, so it may have longer-lasting effects. Unlike most drugs, Versed dosages are based upon the drug's effect rather than your weight.

The dose should be adjusted based on the result of the initial dose, meaning that you'll be given more or less of the drug based on how effective it is. Your ability to tolerate alcohol often provides a hint of your likely tolerance for Versed. If you become intoxicated easily, you may require less medication than someone who can "hold their liquor. Versed is a very useful drug for sedation during procedures, but it must be used in the appropriate setting with trained staff present and electronic monitoring in use for safety.

This medication can cause memory loss and decreased breathing, so it is essential that a trained professional is present to monitor the effects you experience. Versed is a benzodiazepine used as a sedative before medical or dental procedures. Yes, side effects of Versed include drowsiness, loss of memory, and slower breathing. It can also cause a cough. In some instances, Versed can cause agitation, hyperactivity, or combativeness as it wears off.

You should not drive after taking Versed. Versed is a short-acting medicine that lasts between one and six hours, depending on the individual. The drug stays in your system and can be detected on a drug test for two days.

Sign up for our Health Tip of the Day newsletter, and receive daily tips that will help you live your healthiest life. National Institutes of Health, U. National Library of Medicine: MedlinePlus. Midazolam injection. Updated October 27, Comparison of midazolam with fentanyl-midazolam combination during flexible bronchoscopy: A randomized, double-blind, placebo-controlled study.