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Monday, April 15, 2024

Delirium

From Wikipedia, the free encyclopedia
Delirium
SpecialtyPsychiatry, geriatrics, intensive care medicine, neurology
SymptomsAgitation, confusion, drowsiness, hallucinations, delusions, memory problems
Usual onsetAny age, but more often in people aged 65 and above
DurationDays to weeks, sometimes months
TypesHyperactive, hypoactive, mixed level of activity
CausesInconclusive
Risk factorsInfection, chronic health problems, certain medications, neurological problems, sleep deprivation, surgery
Differential diagnosisDementia
TreatmentTreating underlying cause, symptomatic management with medication
MedicationHaloperidol, risperidone, olanzapine, quetiapine

Delirium (formerly acute confusional state, an ambiguous term that is now discouraged) is a specific state of acute confusion attributable to the direct physiological consequence of a medical condition, effects of a psychoactive substance, or multiple causes, which usually develops over the course of hours to days. As a syndrome, delirium presents with disturbances in attention, awareness, and higher-order cognition. People with delirium may experience other neuropsychiatric disturbances, including changes in psychomotor activity (e.g. hyperactive, hypoactive, or mixed level of activity), disrupted sleep-wake cycle, emotional disturbances, disturbances of consciousness, or, altered state of consciousness, as well as perceptual disturbances (e.g. hallucinations and delusions), although these features are not required for diagnosis.

Diagnostically, delirium encompasses both the syndrome of acute confusion and its underlying organic process known as an acute encephalopathy. The cause of delirium may be either a disease process inside the brain or a process outside the brain that nonetheless affects the brain. Delirium may be the result of an underlying medical condition (e.g., infection or hypoxia), side effect of a medication, substance intoxication (e.g., opioids or hallucinogenic deliriants), substance withdrawal (e.g., alcohol or sedatives), or from multiple factors affecting one's overall health (e.g., malnutrition, pain, etc.). In contrast, the emotional and behavioral features due to primary psychiatric disorders (e.g., as in schizophrenia, bipolar disorder) do not meet the diagnostic criteria for 'delirium'.

Delirium may be difficult to diagnose without first establishing a person's usual mental function or 'cognitive baseline'. Delirium can be confused with multiple psychiatric disorders or chronic organic brain syndromes because of many overlapping signs and symptoms in common with dementia, depression, psychosis, etc. Delirium may occur in persons with existing mental illness, baseline intellectual disability, or dementia, entirely unrelated to any of these conditions.

Treatment of delirium requires identifying and managing the underlying causes, managing delirium symptoms, and reducing the risk of complications. In some cases, temporary or symptomatic treatments are used to comfort the person or to facilitate other care (e.g., preventing people from pulling out a breathing tube). Antipsychotics are not supported for the treatment or prevention of delirium among those who are in hospital; however, they may be used in cases where a person has distressing experiences such as hallucinations or if the person poses a danger to themselves or others. When delirium is caused by alcohol or sedative-hypnotic withdrawal, benzodiazepines are typically used as a treatment. There is evidence that the risk of delirium in hospitalized people can be reduced by non-pharmacological care bundles (see Delirium § Prevention). According to the text of DSM-5-TR, although delirium affects only 1–2% of the overall population, 18–35% of adults presenting to the hospital will have delirium, and delirium will occur in 29–65% of people who are hospitalized. Delirium occurs in 11–51% of older adults after surgery, in 81% of those in the ICU, and in 20–22% of individuals in nursing homes or post-acute care settings. Among those requiring critical care, delirium is a risk factor for death within the next year.

Definition

In common usage, delirium can refer to drowsiness, agitation, disorientation, or hallucinations. In medical terminology, however, the core features of delirium include an acute disturbance in attention, awareness, and global cognition.

Although slight differences exist between the definitions of delirium in the DSM-5-TR and ICD-10, the core features are broadly the same. In 2022, the American Psychiatric Association released the fifth edition text revision of the DSM (DSM-5-TR) with the following criteria for diagnosis:

  • A. Disturbance in attention and awareness. This is a required symptom and involves easy distraction, inability to maintain attentional focus, and varying levels of alertness.
  • B. Onset is acute (from hours to days), representing a change from baseline mentation and often with fluctuations throughout the day
  • C. At least one additional cognitive disturbance (in memory, orientation, language, visuospatial ability, or perception)
  • D. The disturbances (criteria A and C) are not better explained by another neurocognitive disorder
  • E. There is evidence that the disturbances above are a "direct physiological consequence" of another medical condition, substance intoxication or withdrawal, toxin, or various combinations of causes

Signs and symptoms

Delirium exists across a range of arousal levels, either as a state between normal wakefulness/alertness and coma (hypoactive) or as a state of heightened psychophysiological arousal (hyperactive). It can also alternate between the two (mixed level of activity). While requiring an acute disturbance in attention, awareness, and cognition, the syndrome of delirium encompasses a broad range of additional neuropsychiatric disturbances.

  • Inattention: A disturbance in attention is required for delirium diagnosis. This may present as an impaired ability to direct, focus, sustain, or shift attention.
  • Memory impairment: The memory impairment that occurs in delirium is often due to an inability to encode new information, largely as a result of having impaired attention. Older memories already in storage are retained without need of concentration, so previously formed long-term memories (i.e., those formed before the onset of delirium) are usually preserved in all but the most severe cases of delirium, though recall of such information may be impaired due to global impairment in cognition.
  • Disorientation: A person may be disoriented to self, place, or time. Additionally, a person may be 'disoriented to situation' and not recognize their environment or appreciate what is going on around them.
  • Disorganized thinking: Disorganized thinking is usually noticed with speech that makes limited sense with apparent irrelevancies, and can involve poverty of speech, loose associations, perseveration, tangentiality, and other signs of a formal thought disorder.
  • Language disturbances: Anomic aphasia, paraphasia, impaired comprehension, agraphia, and word-finding difficulties all involve impairment of linguistic information processing.
  • Sleep/wake disturbances: Sleep disturbances in delirium reflect disruption in both sleep/wake and circadian rhythm regulation, typically characterized by fragmented sleep or even sleep-wake cycle reversal (i.e., active at night, sleeping during the day), including as an early sign preceding the onset of delirium.
  • Psychotic and other erroneous beliefs: Symptoms of psychosis include suspiciousness, overvalued ideation and frank delusions. Delusions are typically poorly formed and less stereotyped than in schizophrenia or Alzheimer's disease. They usually relate to persecutory themes of impending danger or threat in the immediate environment (e.g., being poisoned by nurses).
  • Perceptual disturbances: These can include illusions, which involve the misperception of real stimuli in the environment, or hallucinations, which involve the perception of stimuli that do not exist.
  • Mood lability: Distortions to perceived or communicated emotional states as well as fluctuating emotional states can manifest in delirium (e.g., rapid changes between terror, sadness and joking).
  • Motor activity changes: Delirium has been commonly classified into psychomotor subtypes of hypoactive, hyperactive, and mixed level of activity, though studies are inconsistent as to their prevalence. Hypoactive cases are prone to non-detection or misdiagnosis as depression. A range of studies suggests that motor subtypes differ regarding underlying pathophysiology, treatment needs, functional prognosis, and risk of mortality, though inconsistent subtype definitions and poorer detection of hypoactive subtypes may influence the interpretation of these findings. The notion of unifying hypoactive and hyperactive states under the construct of delirium is commonly attributed to Lipowski.
    • Hyperactive symptoms include hyper-vigilance, restlessness, fast or loud speech, irritability, combativeness, impatience, swearing, singing, laughing, uncooperativeness, euphoria, anger, wandering, easy startling, fast motor responses, distractibility, tangentiality, nightmares, and persistent thoughts (hyperactive sub-typing is defined with at least three of the above).
    • Hypoactive symptoms include decreased alertness, sparse or slow speech, lethargy, slowed movements, staring, and apathy.
    • Mixed level of activity describes instances of delirium where activity level is either normal or fluctuating between hyperactive and hypoactive.

Causes

Delirium arises through the interaction of a number of predisposing and precipitating factors.

Individuals with multiple and/or significant predisposing factors are at high risk for an episode of delirium with a single and/or mild precipitating factor. Conversely, delirium may only result in low risk individuals if they experience a serious or multiple precipitating factors. It is important to note that these factors can change over time, thus an individual's risk of delirium is modifiable (see Delirium § Prevention).

Predisposing factors

Important predisposing factors include the following:

Precipitating factors

Acute confusional state caused by alcohol withdrawal, also known as delirium tremens

Any serious, acute biological factor that affects neurotransmitter, neuroendocrine, or neuroinflammatory pathways can precipitate an episode of delirium in a vulnerable brain. Certain elements of the clinical environment have also been associated with the risk of developing delirium. Some of the most common precipitating factors are listed below:

Pathophysiology

The pathophysiology of delirium is still not well understood, despite extensive research.

Animal models

The lack of animal models that are relevant to delirium has left many key questions in delirium pathophysiology unanswered. Earliest rodent models of delirium used atropine (a muscarinic acetylcholine receptor blocker) to induce cognitive and electroencephalography (EEG) changes similar to delirium, and other anticholinergic drugs, such as biperiden and hyoscine, have produced similar effects. Along with clinical studies using various drugs with anticholinergic activity, these models have contributed to a "cholinergic deficiency hypothesis" of delirium.

Profound systemic inflammation occurring during sepsis is also known to cause delirium (often termed sepsis-associated encephalopathy). Animal models used to study the interactions between prior degenerative disease and overlying systemic inflammation have shown that even mild systemic inflammation causes acute and transient deficits in working memory among diseased animals. Prior dementia or age-associated cognitive impairment is the primary predisposing factor for clinical delirium and "prior pathology" as defined by these new animal models may consist of synaptic loss, abnormal network connectivity, and "primed microglia" brain macrophages stimulated by prior neurodegenerative disease and aging to amplify subsequent inflammatory responses in the central nervous system (CNS).

Cerebrospinal fluid

Studies of cerebrospinal fluid (CSF) in delirium are difficult to perform. Apart from the general difficulty of recruiting participants who are often unable to give consent, the inherently invasive nature of CSF sampling makes such research particularly challenging. However, a few studies have managed to sample CSF from persons undergoing spinal anesthesia for elective or emergency surgery.

There is a 2018 systematic review showed that, broadly, delirium may be associated with neurotransmitter imbalance (namely serotonin and dopamine signaling), reversible fall in somatostatin, and increased cortisol. The leading "neuroinflammatory hypothesis" (where neurodegenerative disease and aging leads the brain to respond to peripheral inflammation with an exaggerated CNS inflammatory response) has been described, but current evidence is still conflicting and fails to concretely support this hypothesis.

Neuroimaging

Neuroimaging provides an important avenue to explore the mechanisms that are responsible for delirium. Despite progress in the development of magnetic resonance imaging (MRI), the large variety in imaging-based findings has limited our understanding of the changes in the brain that may be linked to delirium. Some challenges associated with imaging people diagnosed with delirium include participant recruitment and inadequate consideration of important confounding factors such as history of dementia and/or depression, which are known to be associated with overlapping changes in the brain also observed on MRI.

Evidence for changes in structural and functional markers include: changes in white-matter integrity (white matter lesions), decreases in brain volume (likely as a result of tissue atrophy), abnormal functional connectivity of brain regions responsible for normal processing of executive function, sensory processing, attention, emotional regulation, memory, and orientation, differences in autoregulation of the vascular vessels in the brain, reduction in cerebral blood flow and possible changes in brain metabolism (including cerebral tissue oxygenation and glucose hypometabolism). Altogether, these changes in MRI-based measurements invite further investigation of the mechanisms that may underlie delirium, as a potential avenue to improve clinical management of people with this condition.

Neurophysiology

Electroencephalography (EEG) allows for continuous capture of global brain function and brain connectivity, and is useful in understanding real-time physiologic changes during delirium. Since the 1950s, delirium has been known to be associated with slowing of resting-state EEG rhythms, with abnormally decreased background alpha power and increased theta and delta frequency activity.

From such evidence, a 2018 systematic review proposed a conceptual model that delirium results when insults/stressors trigger a breakdown of brain network dynamics in individuals with low brain resilience (i.e. people who already have underlying problems of low neural connectivity and/or low neuroplasticity like those with Alzheimer's disease).

Neuropathology

Only a handful of studies exist where there has been an attempt to correlate delirium with pathological findings at autopsy. One research study has been reported on 7 people who died during ICU admission. Each case was admitted with a range of primary pathologies, but all had acute respiratory distress syndrome and/or septic shock contributing to the delirium, 6 showed evidence of low brain perfusion and diffuse vascular injury, and 5 showed hippocampal involvement. A case-control study showed that 9 delirium cases showed higher expression of HLA-DR and CD68 (markers of microglial activation), IL-6 (cytokines pro-inflammatory and anti-inflammatory activities) and GFAP (marker of astrocyte activity) than age-matched controls; this supports a neuroinflammatory cause to delirium, but the conclusions are limited by methodological issues.

A 2017 retrospective study correlating autopsy data with MMSE scores from 987 brain donors found that delirium combined with a pathological process of dementia accelerated MMSE score decline more than either individual process.

Diagnosis

The DSM-5-TR criteria are often the standard for diagnosing delirium clinically. However, early recognition of delirium's features using screening instruments, along with taking a careful history, can help in making a diagnosis of delirium. A diagnosis of delirium generally requires knowledge of a person's baseline level of cognitive function. This is especially important for treating people who have neurocognitive or neurodevelopmental disorders, whose baseline mental status may be mistaken as delirium.

General settings

Guidelines recommend that delirium should be diagnosed consistently when present. Much evidence reveals that in most centers delirium is greatly under-diagnosed. A systematic review of large scale routine data studies reporting data on delirium detection tools showed important variations in tool completion rates and tool positive score rates. Some tools, even if completed at high rates, showed delirium positive score rates that there much lower than the expected delirium occurrence level, suggesting low sensitivity in practice.

There is evidence that delirium detection and coding rates can show improvements in response to guidelines and education; for example, whole country data in England and Scotland (sample size 7.7M patients per year) show that there were large increases (3-4 fold) in delirium coding between 2012 and 2020. Delirium detection in general acute care settings can be assisted by the use of validated delirium screening tools. Many such tools have been published, and they differ in a variety of characteristics (e.g., duration, complexity, and need for training). It is also important to ensure that a given tool has been validated for the setting where it is being used.

Examples of tools in use in clinical practice include:

  • Confusion Assessment Method (CAM), including variants such as the 3-Minute Diagnostic Interview for the CAM (3D-CAM) and brief CAM (bCAM)
  • Delirium Observation Screening Scale (DOS)
  • Nursing Delirium Screening Scale (Nu-DESC)
  • Recognizing Acute Delirium As part of your Routine (RADAR)
  • 4AT (4 A's Test)
  • Delirium Diagnostic Tool-Provisional (DDT-Pro), also for subsyndromal delirium

Intensive care unit

People who are in the ICU are at greater risk of delirium, and ICU delirium may lead to prolonged ventilation, longer stays in the hospital, increased stress on family and caregivers, and an increased chance of death. In the ICU, international guidelines recommend that every person admitted gets checked for delirium every day (usually twice or more a day) using a validated clinical tool. Key elements of detecting delirium in the ICU are whether a person can pay attention during a listening task and follow simple commands. The two most widely used are the Confusion Assessment Method for the ICU (CAM-ICU) and the Intensive Care Delirium Screening Checklist (ICDSC). Translations of these tools exist in over 20 languages and are used ICUs globally with instructional videos and implementation tips available. For children in need of intensive care there are validated clinical tools adjusted according to age. The recommended tools are preschool and pediatric Confusion Assessment Methods for the ICU (ps/pCAM-ICU) or the Cornell Assessment for Pediatric Delirium (CAPD) as the most valid and reliable delirium monitoring tools in critically ill children or adolescents.

More emphasis is placed on regular screening over the choice of tool used. This, coupled with proper documentation and informed awareness by the healthcare team, can affect clinical outcomes. Without using one of these tools, 75% of ICU delirium can be missed by the healthcare team, leaving the person without any likely interventions to help reduce the duration of delirium.

Differential diagnosis

There are conditions that might have similar clinical presentations to those seen in delirium. These include dementia, depression, psychosis, catatonia, and other conditions that affect cognitive function.

  • Dementia: This group of disorders is acquired (non-congenital) with usually irreversible cognitive and psychosocial functional decline. Dementia usually results from an identifiable degenerative brain disease (e.g., Alzheimer disease or Huntington's disease), requires chronic impairment (versus acute onset in delirium), and is typically not associated with changes in level of consciousness. Dementia is different from delirium in that dementia lasts long-term while delirium lasts short-term.
  • Depression: Similar symptoms exist between depression and delirium (especially the hypoactive subtype). Gathering a history from other caregivers can clarify baseline mentation.
  • Psychosis: In general, people with primary psychosis have intact cognitive function; however, primary psychosis can mimic delirium when it presents with disorganized thoughts and mood dysregulation. This is particularly true in the condition known as delirious mania.
  • Other mental illnesses: Some mental illnesses, such as a manic episode of bipolar disorder, depersonalization disorder, or other dissociative conditions, can present with features similar to that of delirium. Such condition, however, would not qualify for a diagnosis of delirium per DSM-5-TR criterion D (i.e., fluctuating cognitive symptoms occurring as part of a primary mental disorder are results of the said mental disorder itself), while physical disorders (e.g., infections, hypoxia, etc.) can precipitate delirium as a mental side-effect/symptom.

Prevention

Treating delirium that is already established is challenging and for this reason, preventing delirium before it begins is ideal. Prevention approaches include screening to identify people who are at risk, and medication-based and non-medication based (non-pharmacological) treatments.

An estimated 30–40% of all cases of delirium could be prevented in cognitively at-risk populations, and high rates of delirium reflect negatively on the quality of care. Episodes of delirium can be prevented by identifying hospitalized people at risk of the condition. This includes individuals over age 65, with a cognitive impairment, undergoing major surgery, or with severe illness. Routine delirium screening is recommended in such populations. It is thought that a personalized approach to prevention that includes different approaches together can decrease rates of delirium by 27% among the elderly.

In 1999, Sharon K. Inouye at Yale University, founded the Hospital Elder Life Program (HELP)  which has since become recognized as a proven model for preventing delirium. HELP prevents delirium among the elderly through active participation and engagement with these individuals. There are two working parts to this program, medical professionals such as a trained nurse, and volunteers, who are overseen by the nurse. The volunteer program equips each trainee with the adequate basic geriatric knowledge and interpersonal skills to interact with patients. Volunteers perform the range of motion exercises, cognitive stimulation, and general conversation with elderly patients who are staying in the hospital. Alternative effective delirium prevention programs have been developed, some of which do not require volunteers.

Prevention efforts often fall on caregivers. Caregivers often have a lot expected of them and this is where socioeconomic status plays a role in prevention. If prevention requires constant mental stimulation and daily exercise, this takes time out of the caregiver's day. Based on socioeconomic classes, this may be valuable time that would be used working to support the family. This leads to a disproportionate amount of individuals who experience delirium being from marginalized identities. Programs such as the Hospital Elder Life Program can attempt to combat these societal issues by providing additional support and education about delirium that may not otherwise be accessible.

Non-pharmacological

Delirium may be prevented and treated by using non-pharmacologic approaches focused on risk factors, such as constipation, dehydration, low oxygen levels, immobility, visual or hearing impairment, sleep disturbance, functional decline, and by removing or minimizing problematic medications. Ensuring a therapeutic environment (e.g., individualized care, clear communication, adequate reorientation and lighting during daytime, promoting uninterrupted sleep hygiene with minimal noise and light at night, minimizing room relocation, having familiar objects like family pictures, providing earplugs, and providing adequate nutrition, pain control, and assistance toward early mobilization) may also aid in preventing delirium. Research into pharmacologic prevention and treatment is weak and insufficient to make proper recommendations.

Pharmacological

Melatonin and other pharmacological agents have been studied for delirium prevention, but evidence is conflicting. Avoidance or cautious use of benzodiazepines has been recommended for reducing the risk of delirium in critically ill individuals. It is unclear if the medication donepezil, a cholinesterase inhibitor, reduces delirium following surgery. There is also no clear evidence to suggest that citicoline, methylprednisolone, or antipsychotic medications prevent delirium. A review of intravenous versus inhalational maintenance of anaesthesia for postoperative cognitive outcomes in elderly people undergoing non-cardiac surgery showed little or no difference in postoperative delirium according to the type of anaesthetic maintenance agents in five studies (321 participants). The authors of this review were uncertain whether maintenance of anaesthesia with propofol-based total intravenous anaesthesia (TIVA) or with inhalational agents can affect the incidence rate of postoperative delirium.

Interventions for preventing delirium in long-term care or hospital

The current evidence suggests that software-based interventions to identify medications that could contribute to delirium risk and recommend a pharmacist's medication review probably reduces incidence of delirium in older adults in long-term care. The benefits of hydration reminders and education on risk factors and care homes' solutions for reducing delirium is still uncertain.

For inpatients in a hospital setting, numerous approaches have been suggested to prevent episodes of delirium including targeting risk factors such as sleep deprivation, mobility problems, dehydration, and impairments to a person's sensory system. Often a 'multicomponent' approach by an interdisciplinary team of health care professionals is suggested for people in the hospital at risk of delirium, and there is some evidence that this may decrease to incidence of delirium by up to 43% and may reduce the length of time that the person is hospitalized.

Treatment

Most often, delirium is reversible; however, people with delirium require treatment for the underlying cause(s) and often to prevent injury and other poor outcomes directly related to delirium.

Treatment of delirium requires attention to multiple domains including the following:

  • Identify and treat the underlying medical disorder or cause(s)
  • Addressing any other possible predisposing and precipitating factors that might be disrupting brain function
  • Optimize physiology and conditions for brain recovery (e.g., oxygenation, hydration, nutrition, electrolytes, metabolites, medication review)
  • Detect and manage distress and behavioral disturbances (e.g., pain control)
  • Maintaining mobility
  • Provide rehabilitation through cognitive engagement and mobilization
  • Communicate effectively with the person experiencing delirium and their carers or caregivers
  • Provide adequate follow-up including consideration of possible dementia and post-traumatic stress.

Multidomain interventions

These interventions are the first steps in managing acute delirium, and there are many overlaps with delirium preventative strategies. In addition to treating immediate life-threatening causes of delirium (e.g., low O2, low blood pressure, low glucose, dehydration), interventions include optimizing the hospital environment by reducing ambient noise, providing proper lighting, offering pain relief, promoting healthy sleep-wake cycles, and minimizing room changes. Although multicomponent care and comprehensive geriatric care are more specialized for a person experiencing delirium, several studies have been unable to find evidence showing they reduce the duration of delirium.

Family, friends, and other caregivers can offer frequent reassurance, tactile and verbal orientation, cognitive stimulation (e.g. regular visits, familiar objects, clocks, calendars, etc.), and means to stay engaged (e.g. making hearing aids and eyeglasses readily available). Sometimes verbal and non-verbal deescalation techniques may be required to offer reassurances and calm the person experiencing delirium. Restraints should rarely be used as an intervention for delirium. The use of restraints has been recognized as a risk factor for injury and aggravating symptoms, especially in older hospitalized people with delirium. The only cases where restraints should sparingly be used during delirium is in the protection of life-sustaining interventions, such as endotracheal tubes.

Another approached called the "T-A-DA (tolerate, anticipate, don't agitate) method" can be an effective management technique for older people with delirium, where abnormal behaviors (including hallucinations and delusions) are tolerated and unchallenged, as long as caregiver safety and the safety of the person experiencing delirium is not threatened. Implementation of this model may require a designated area in the hospital. All unnecessary attachments are removed to anticipate for greater mobility, and agitation is prevented by avoiding excessive reorientation/questioning.

Medications

The use of medications for delirium is generally restricted to managing its distressing or dangerous neuropsychiatric disturbances. Short-term use (one week or less) of low-dose haloperidol is among the more common pharmacological approaches to delirium. Evidence for effectiveness of atypical antipsychotics (e.g. risperidone, olanzapine, ziprasidone, and quetiapine) is emerging, with the benefit for fewer side effects. Use antipsychotic drugs with caution or not at all for people with conditions such as Parkinson's disease or dementia with Lewy bodies. Evidence for the effectiveness of medications (including antipsychotics and benzodiazepines) in treating delirium is weak.

Benzodiazepines can cause or worsen delirium, and there is no reliable evidence of efficacy for treating non-anxiety-related delirium. Similarly, people with dementia with Lewy bodies may have significant side effects with antipsychotics, and should either be treated with a none or small doses of benzodiazepines.

The antidepressant trazodone is occasionally used in the treatment of delirium, but it carries a risk of over-sedation, and its use has not been well studied.

For adults with delirium that are in the ICU, medications are used commonly to improve the symptoms. Dexmedetomidine may shorten the length of the delirium in adults who are critically ill, and rivastigmine is not suggested. For adults with delirium who are near the end of their life (on palliative care) high quality evidence to support or refute the use of most medications to treat delirium is not available. Low quality evidence indicates that the antipsychotic medications risperidone or haloperidol may make the delirium slightly worse in people who are terminally ill, when compared to a placebo treatment. There is also moderate to low quality evidence to suggest that haloperidol and risperidone may be associated with a slight increase in side effects, specifically extrapyramidal symptoms, if the person near the end of their life has delirium that is mild to moderate in severity.

Prognosis

There is substantial evidence that delirium results in long-term poor outcomes in older persons admitted to hospital. This systematic review only included studies that looked for an independent effect of delirium (i.e., after accounting for other associations with poor outcomes, for example co-morbidity or illness severity).

In older persons admitted to hospital, individuals experiencing delirium are twice as likely to die than those who do not (meta-analysis of 12 studies). In the only prospective study conducted in the general population, older persons reporting delirium also showed higher mortality (60% increase). A large (N=82,770) two-centre study in unselected older emergency population found that delirium detected as part of normal care using the 4AT tool was strongly linked to 30-day mortality, hospital length of stay, and days at home in the year following the 4AT test date.

Institutionalization was also twice as likely after an admission with delirium (meta-analysis of seven studies). In a community-based population examining individuals after an episode of severe infection (though not specifically delirium), these persons acquired more functional limitations (i.e., required more assistance with their care needs) than those not experiencing infection. After an episode of delirium in the general population, functional dependence increased threefold.

The association between delirium and dementia is complex. The systematic review estimated a 13-fold increase in dementia after delirium (meta-analysis of two studies). However, it is difficult to be certain that this is accurate because the population admitted to hospital includes persons with undiagnosed dementia (i.e., the dementia was present before the delirium, rather than caused by it). In prospective studies, people hospitalised from any cause appear to be at greater risk of dementia and faster trajectories of cognitive decline, but these studies did not specifically look at delirium. In the only population-based prospective study of delirium, older persons had an eight-fold increase in dementia and faster cognitive decline. The same association is also evident in persons already diagnosed with Alzheimer's dementia.

Recent long-term studies showed that many people still meet criteria for delirium for a prolonged period after hospital discharge, with up to 21% of people showing persistent delirium at 6 months post-discharge.

Dementia in ICU survivors

Between 50% and 70% of people admitted to the ICU have permanent problems with brain dysfunction similar to those experienced by people with Alzheimer's or those with a traumatic brain injury, leaving many ICU survivors permanently disabled. This is a distressing personal and public health problem and continues to receive increasing attention in ongoing investigations.

The implications of such an "acquired dementia-like illness" can profoundly debilitate a person's livelihood level, often dismantling his/her life in practical ways like impairing one's ability to find a car in a parking lot, complete shopping lists, or perform job-related tasks done previously for years. The societal implications can be enormous when considering work-force issues related to the inability of wage-earners to work due to their own ICU stay or that of someone else they must care for.

Epidemiology

The highest rates of delirium (often 50–75% of people) occur among those who are critically ill in the intensive care unit (ICU). This was historically referred to as "ICU psychosis" or "ICU syndrome"; however, these terms are now widely disfavored in relation to the operationalized term ICU delirium. Since the advent of validated and easy-to-implement delirium instruments for people admitted to the ICU such as the Confusion Assessment Method for the ICU (CAM-ICU) and the Intensive Care Delirium Screening Checklist (ICDSC), it has been recognized that most ICU delirium is hypoactive, and can easily be missed unless evaluated regularly. The causes of delirium depend on the underlying illnesses, new problems like sepsis and low oxygen levels, and the sedative and pain medicines that are nearly universally given to all ICU patients. Outside the ICU, on hospital wards and in nursing homes, the problem of delirium is also a very important medical problem, especially for older patients.

The most recent area of the hospital in which delirium is just beginning to be monitored routinely in many centers is the Emergency Department, where the prevalence of delirium among older adults is about 10%. A systematic review of delirium in general medical inpatients showed that estimates of delirium prevalence on admission ranged 10–31%. About 5–10% of older adults who are admitted to hospital develop a new episode of delirium while in hospital. Rates of delirium vary widely across general hospital wards. Estimates of the prevalence of delirium in nursing homes are between 10% and 45%.

Society and culture

Delirium is one of the oldest forms of mental disorder known in medical history. The Roman author Aulus Cornelius Celsus used the term to describe mental disturbance from head trauma or fever in his work De Medicina. Sims (1995, p. 31) points out a "superb detailed and lengthy description" of delirium in "The Stroller's Tale" from Charles Dickens' The Pickwick Papers. Historically, delirium has also been noted for its cognitive sequelae. For instance, the English medical writer Philip Barrow noted in 1583 that if delirium (or "frensy") resolves, it may be followed by a loss of memory and reasoning power.

Costs

In the US, the cost of a hospital admission for people with delirium is estimated at between $16k and $64k, suggesting the national burden of delirium may range from $38 bn to $150 bn per year (2008 estimate). In the UK, the cost is estimated as £13k per admission.

Altered state of consciousness

From Wikipedia, the free encyclopedia
https://en.wikipedia.org/wiki/Altered_state_of_consciousness

An altered state of consciousness (ASC), also called an altered state of mind or mind alteration, is any condition which is significantly different from a normal waking state. By 1892, the expression was in use in relation to hypnosis, though there is an ongoing debate as to whether hypnosis is to be identified as an ASC according to its modern definition. The next retrievable instance, by Max Mailhouse from his 1904 presentation to conference, however, is unequivocally identified as such, as it was in relation to epilepsy, and is still used today. In academia, the expression was used as early as 1966 by Arnold M. Ludwig and brought into common usage from 1969 by Charles Tart. It describes induced changes in one's mental state, almost always temporary. A synonymous phrase is "altered state of awareness".

Definitions

There is no general definition of an altered state of consciousness, as any definitional attempt would first have to rely on a definition of a normal state of consciousness. Attempts to define the term can however be found in philosophy, psychology and neuroscience. There is no final consensus on what the most accurate definition is. The best-established and latest definitions are provided below.

Arnold M. Ludwig attempted a first definition in 1966.

An altered state is any mental state(s), induced by various physiological, psychological, or pharmacological maneuvers or agents, which can be recognized subjectively by the individual himself (or by an objective observer of the individual) as representing a sufficient deviation in subjective experience of psychological functioning from certain general norms for that individual during alert, waking consciousness.

Starting from this, Charles Tart focuses his definition on the subjective experience of a state of consciousness and its deviation from a normal waking state.

Altered states of consciousness are alternate patterns or configurations of experience, which differ qualitatively from a baseline state.

Farthing's definition of an altered state of consciousness (ASC) is based on Charles Tart's terminology. Charles Tart described an altered state of consciousness as a profound change in the "overall pattern of subjective experiences". In order to define an ASC, Tart focuses on the importance of subjective experience.

Farthing adds to his definition that an ASC is short-termed or at least reversible and that it might not even be recognized as an ASC at that moment. His definition relies only on subjective experience, leaving aside behavioral changes and physiological response.

An altered state of consciousness (ASC) may be defined as a temporary change in the overall pattern of subjective experience, such that the individual believes that his or her mental functioning is distinctly different from certain general norms for his or her normal waking state of consciousness. (Farthing, 1992, p. 205)

He lists fourteen dimensions of changed subjective experience. To account for an ASC, multiple dimensions need to be altered.

A recent working definition for empirical research is based on these previous definitions and provided by Schmidt.

[Translated from German]: As a working definition for neuroscientific research, it might suffice to presume that most people have a strong intuition concerning which variability in their everyday wakeful state feels normal to them. This variability of experience is considered as normal fluctuation, while any state that is experienced to diverge significantly from it can be called an ASC. From an experimental perspective, it is also reasonable to compare ASC conditions to a baseline state – a state subjectively judged as average, or normal. The comparison with a 'normal' baseline requires that the ASC under investigation is of relatively short duration (minutes to hours), which differentiates ASCs from most pathological conditions. Importantly, it has been emphasized that an ASC is not a mere quantitative change in a single cognitive function (e.g. elevated arousal). Instead, it is a multidimensional phenomenon. Thereby, the relative intensity of multiple consciousness aspects constitutes a 'phenomenological pattern' characterizing a particular state. Such 'patterns' have also been referred to as relative changes in the '(basic) dimensions of consciousness'. For empirical research, such patterns correspond to a multivariate combination of independent 'consciousness factors', which can be quantified via questionnaires. The 'phenomenological pattern' results from the factor structure of the applied psychometric assessment, i.e. the individual ratings, or factor scores, of a questionnaire.

History

History of utilization of ASCs

Altered states of consciousness might have been employed by humans as early as 30,000 years ago. Mind-altering plants and/or excessive dancing were used to attain an ecstatic or mystic state. Examples of early religious use of altered states of consciousness are the rites of Dionysos and the Eleusinian Mysteries, as well as yoga and meditation. Followers of various shamanic traditions "enter altered states of consciousness in order to serve their community." Terence McKenna has suggested that the use of psychedelic mushrooms in prehistoric times has led to the "evolution of human language and symbol use". Some theorists propose that mind-altering substances, such as soma, might have pushed the formation of some of the world's main religions.

Meditation in its various forms is being rediscovered by modern psychology because of its therapeutic potential and its ability to "enable the activity of the mind to settle down". In psychotherapy, techniques like hypnosis and meditation support psychological processes.

History of the science and theoretical-modelling

Due to the behaviourist paradigm in psychology altered states of consciousness were dismissed as a field of scientific inquiry during the early 20th century. They were pathologized and merely seen as symptoms of intoxication or demonic possession.

Their return into psychology began with Wiliam James' interest into a variety of altered states, such as "mystical experiences and drug-induced states". James' investigations into first-person-subjective-experience contributed to the reconsideration of introspection as a valuable research method in the academic community.

The social change of the turbulent 1960s has decisively led to a change of the scientific perspective to the point that introspection as a scientific method and ASCs as valid realms of experience became more widely accepted. Foundations for the research have been laid out by various scientists such as Abraham Maslow, Walter N. Pahnke, Stanislav Grof and Charles Tart. They focused on seemingly beneficial aspects of ASCs such as their potential to "promote creativity or treat addiction". Rather oppressive states such as dissociation from trauma were neglected.

The findings of the famous Good Friday Experiment by Pahnke suggest that mystical experiences can be triggered by psilocybin. Later investigations by Rick Doblin found that participants valued those experiences as "spiritual high points of their lives".

In the midst of the rise of new-age subculture Stanislav Grof and others formed the new field of transpersonal psychology, which emphasized "the importance of individual human experience, validity of mystical and spiritual experience, interconnectedness of self with others and the world and potential of self-transformation".

Abraham Maslow's research on peak experiences, as moments of "highest happiness and fulfillment", further contributed to the depathologization of altered states.

A first summary of the existing literature was carried out by Charles T. Tart in his book Altered the States of Consciousness, which led to a more common use of the term. Tart coined the key terms discrete and baseline states of consciousness and thought about a general classification system for ASCs. He also called for "state specific sciences" in which researchers should do science on ASCs from within such states.

Classification

A simple classification scheme for ASC. Sleep and dream states are distinguished from waking consciousness since they account for substantially different ways of the ability of memory formation and retrieval. Psychiatric diseases that go along with persistent changes of consciousness, like schizophrenia, are covered with the term "pathological conditions". In contrast, the classification scheme includes intended and induced ASCs as well as general fluctuations of neurotransmission, which are reversible and short-termed. One step further the graph suggests splitting induced ASCs in persistent and reversible states. Translated from German Schmidt & Majic.

A classification of Altered States of Consciousness is helpful for comparing or differentiating induced ASCs and other variations of consciousness. Various researchers have attempted the classification into a broader framework. The attempts of classification discussed in the following focus on slightly different aspects of ASCs. Several authors suggested classification schemata with regard to the genesis of altered states and with regard to the type of experiences:

A classification with five categories was suggested by Dieter Vaitl to distinguish ASCs according to how they were induced:

  • Pathological (Epilepsy, brain damage)
  • Pharmacological (psychoactive substances)
  • Physical and physiological (fasting and sex)
  • Psychological (music, meditation, hypnosis)
  • Spontaneous (day-dreaming and near death experience)

Vaitl further suggests four basic aspects of experiences: (1) activation (2) awareness span (3) self-awareness (4) sensory dynamics. Alternatively Roland Fischer suggests a classification along ergotropic (i.e., ecstasy) or trophotropic (i.e., meditation) properties. The work of Adolph Dittrich aimed to empirically determine common underlying dimensions of consciousness alterations induced by different methods, such as drugs or non-pharmacological methods. He suggested three basic dimensions, which were termed: (1) oceanic boundlessness (2) dread of ego dissolution (3) visionary restructuralization. Further, Ken Wilber proposes a multidimensional system and adds that the individual experience of an ASC is shaped by a person's unique psychological development.

Michael Winkelman identifies four different "modes of consciousness": (1) the waking mode (2) the deep sleep mode (3) the REM sleep / dreaming mode (4) the integrative mode. Within this framework, many ASCs (psychedelics, hypnosis, meditation, etc.) are defined as belonging to the integrative mode.

Induction methods

Pharmacological

An altered state of consciousness may be defined as a short-term change in the general configuration of one's individual experience, such that the rational functioning is clearly altered from one's usual state of consciousness. There are many ways that one's consciousness can be altered, such as by using psychoactive drugs, which are defined as chemical substances that pass through the blood-brain barrier and disturb brain function, causing changes in awareness, attitude, consciousness, and behavior.

Cannabis is a psychoactive drug that is known to alter the state of consciousness. Cannabis alters mental activity, memory, and pain perception. One who is under the influence of cannabis may experience degrees of paranoia, increased sensitivity, and delayed reactions not normal for their usual conscious state. A 2009 review of anxiety and cannabis studies concluded that "frequent cannabis users appear to have higher levels of anxiety than non-users," and that "a considerable number of subjects developed anxiety disorders before the first symptoms of cannabis dependence." That led researchers to believe that anxiety-prone people tend to use cannabis as a self-prescribed anxiety medicine, opposing the idea that cannabis is what's causing the anxiety.

MDMA (ecstasy) is a drug that also alters one's state of consciousness. The state of consciousness brought about by MDMA ingestion includes a rise in positive feelings and a reduction in negative feelings (Aldridge, D., & Fachner, J. ö. 2005). Users' emotions are increased and inhibitions lowered, often accompanied by a sensation of intimacy or connection with other people.

Opioids are a class of drugs that alter consciousness. Examples of opioids include heroin, morphine, hydrocodone, and oxycodone. Opioids produce analgesia and often feelings of euphoria in users. Opioid abuse may result in decreased production of endorphins in the brain, natural pain relievers whose effects may be heightened by drugs.

Cocaine alters one's state of consciousness. Cocaine affects the neurotransmitters that nerves use to communicate with each other. Cocaine inhibits the reuptake of norepinephrine, serotonin, dopamine, and other neurotransmitters in the synapse, resulting in an altered state of consciousness or a "high" (Aldridge, D., & Fachner, J. ö. 2005).

Lysergic acid diethylamide, or LSD, activates serotonin receptors (the amine transmitter of nerve urges) in brain matter. LSD acts on certain serotonin receptors, and its effects are most prominent in the cerebral cortex, an area involved in attitude, thought, and insight, which obtains sensory signs from all parts of the body. LSD's main effects are emotional and psychological. The ingester's feelings may alter quickly through a range from fear to ecstasy (Humphrey, N. 2001). This may cause one to experience many levels of altered consciousness. It has also been shown to induce ego death (or ego dissolution).

Alcohol alters consciousness by shifting levels of neurotransmitters. Neurotransmitters are endogenous chemicals that transmit signals across a synapse from one neuron (nerve cell) to another "target" cell (often another neuron). Neurotransmitters can cause inhibitory or excitatory effects on the "target" cell they are affecting. Alcohol increases the effect of the neurotransmitter GABA (gamma-Aminobutyric acid) in the brain. GABA causes slow actions and inaudible verbal communication that often occur in alcoholics. Alcohol also decreases the excitatory neurotransmitter glutamate. Suppressing this stimulant results in a similar type of physiological slowdown. In addition to increasing the GABA and decreasing the glutamate in the brain, alcohol increases the amount of the chemical dopamine in the brain, which is one of the addictive causes of alcoholism.

Non-pharmacological

Altered states of consciousness may also be induced by:

Emotions influence behavior that alters the state of consciousness. Emotions can be influenced by various stimuli.

Pathologies/other

Pathological or accidental induction may refer to unforeseen events or illnesses. According to Jeffrey R. Avner, professor of clinical pediatrics, a crucial element to understanding accidental and pathological causes of altered states of consciousness (ASCs) is that it begins with reduced self-awareness followed by reduced awareness in the environment (2006). Those with personal experience of conditions such as Depersonalisation often cite the opposite, that it is an increased awareness of the environment and the self that results in altered states of consciousness. When the reduction of self-awareness and environmental awareness take effect, they produce altered states of consciousness. The specific conditions below provide clarity on the types of conditions compromise accidental and pathological causes.

Traumatic experience

The first condition, traumatic experience, is defined as a lesion caused by an external force (Trauma. (n.d.) In Merriam-Webster Dictionary online, 2013). Examples include impact to the brain caused by blunt force (i.e., a car accident). The reason a traumatic experience causes altered states of consciousness is that it changes how the brain works. The external impact diverts the blood flow from the front of the brain to other areas. The front of the brain is known as the prefrontal cortex responsible for analytical thought (Kunsman, 2012). When the damage becomes uncontrollable, the patient experiences changes in behavior and impaired self-awareness. This is exactly when an altered state of consciousness is experienced.

Epilepsy

Another common cause of ASCs is epilepsy. According to Medlineplus epilepsy is as a brain disorder that causes seizures (2013). During the seizure, the patient will experience hallucinations and loss of mental control, causing temporary dissociation from reality. A study that was conducted with six epileptic patients and used functional magnetic resonance imaging (fMRI) detected how the patients did indeed experience hallucinations while a seizure is occurring. This not only altered the patient's behavioral pattern but also made them dissociate from reality during that particular time frame.

Oxygen deficiency

Oxygen deficiency impacts the brain, which is why ASCs can occur when there is oxygen deprivation in an environment.

Infections

In addition to oxygen deprivation or deficiency, infections are a common pathological cause of ASC. A prime example of an infection is meningitis. The medical website WEBMD states that meningitis is an infection that causes the coverings of the brain to swell. This particular infection occurs in children and young adults. This infection is primarily viral. Viral meningitis causes ASC and its symptoms include fevers and seizures (2010). The Impairment becomes visible the moment seizures begin to occur, this is when the patient enters the altered state of consciousness.

Sleep deprivation

Sleep deprivation is also associated with ASCs, and can provoke seizures due to fatigue. Sleep deprivation can be chronic or short-term depending on the severity of the patient's condition. Many patients report hallucinations because sleep deprivation impacts the brain. An MRI study conducted at Harvard Medical School in 2007 found that a sleep-deprived brain was not capable of being in control of its sensorimotor functions, leading to impaired self-awareness. Patients were also much clumsier than if they had not been experiencing sleep deprivation.

Fasting

Fasting is another form of deprivation. Fasting can occur because of religious purposes or from psychological conditions such as anorexia. Fasting refers to the ability to willingly refrain from food and possibly drinks as well. The dissociation caused by fasting is not only life-threatening but it is the reason why extended fasting periods can lead to ASC. Thus, the temporary dissociation from reality allows fasting to fall into the category of an ASC following the definition provided by Avner (2006).

Psychosis

Another pathological cause is psychosis, otherwise known as a psychotic episode. Psychotic episodes often include delusions, paranoia, derealization, depersonalization, and hallucinations (Revonsuo et al., 2008). Studies have not been able to clearly identify when a person is reaching a higher level of risk for a psychotic episode (Schimmelmann, B., Walger, P., & Schultze-Lutter, F., 2013), but the earlier people are treated for psychosis the more likely they are to avoid the devastating consequences which could lead to a psychotic disorder (Schimmelmann, B., Walger, P., & Schultze-Lutter, F., 2013). Unfortunately, there are very few studies which have thoroughly investigated psychotic episodes, and the ability to predict this disorder remains unclear. (Schimmelmann, B., Walger, P., & Schultze-Lutter, F., 2013).

Reviewing the previous conditions for accidental and pathological causes, we can come to understand that all of these accidental or pathological causes share the component of reduced self-awareness. Therefore, ASCs cannot only be caused naturally but they can be induced intentionally with methods including hypnosis meditation, amongst others. There are also ASCs which are caused by less recreational purposes; people who utilize illegal substances, or heavy dosages of medications, as well as large amounts of alcohol, can indeed comply with the definition of an ASC (Revonsuo et al., 2008).

Neurobiological models of altered state experiences

Entropic brain hypothesis

The entropic brain hypothesis by Robin Carhart-Harris in 2014 is a theory informed by neuroimaging research that uses the hallucinogen-induced neurological state to make inferences about other states of consciousness. The expression "entropy" is applied here in the context of states of consciousness and their associated neurodynamics, where high entropy means a high level of disorder. The theory proposes a general distinction etween two fundamentally different modes of cognition, referred to as primary and secondary consciousness.

Primary consciousness is associated with unconstrained cognition and less ordered (higher-entropy) neurodynamics that preceded the development of modern, normal waking consciousness in adults. Examples include the psychedelic state, the rapid eye movement sleep (REM) state or the onset phase of psychosis. Secondary consciousness is associated with constrained cognition and more ordered neurodynamics. Examples include normal waking consciousness, the anesthetized or the depressed state.

The theory further proposes that via pharmacological induction of psychedelic substances psilocybin, the brain is able to enter into the primary state of consciousness (the psychedelic state) from normal waking consciousness. This "phase transition" between these two fundamentally different poles of consciousness is facilitated by a collapse of the normally highly organized activity within the default mode network (DMN) and a decoupling between the DMN and the medial temporal lobes (MTLs), which are normally significantly coupled. The DMN is closely associated with higher-order cognitive functions such as supporting the neurological basis for the self (e.g. self-reflection, subjectivity, introspection), thinking about others (e.g. theory of mind), remembering the past and thinking about the future (e.g. episodic memory). Task-positive networks are associated with the inverse of these things e.g., focus on and scrutiny of the external world.

The entropic brain hypothesis emphasizes the great research potential of the psychedelic state of mind for gaining more insight into general human consciousness.

CSTC-loop

Extensive scientific investigation on altered states of consciousness and their relationship to drug interactions with receptors in the brain have been performed. Particularly the study of the neurotransmitter serotonin and the effects of psychedelic drugs on the brain has been intensively researched over the past sixty years. It has been hypothesized that hallucinogens act either as an antagonist or an agonist at 5-HT2A (serotonin-2A) receptors and will elicit a state that shares some common phenomenological features with early acute stages of the group of schizophrenia disorders.

Findings implicate that abnormalities of serotonin function and the serotonergic system could be responsible for psychiatric disorders such as the spectrum of schizophrenia (gating) disorders and therefore, that serotonin agonist or antagonists might be useful in the treatment of disorders such as schizophrenia. To investigate the underlying causative neurotransmitter mechanisms of this phenomenon, the CSTC (cortico-striato-thalamo-cortical) loop model has been formulated based on empirical neurobiological work. It is indicated that the common hypofrontality (underactivation of frontal brain regions) and cortical activation pattern induced by serotonergic and glutamatergic hallucinogens is due to a common disruption of thalamic gating of sensory and cognitive information. The CSTC feedback loop plays a major role in gating or filtering out external and internal information to the cortex. Thereby it influences the regulation of the level of awareness and attention.

Disruption of the CSTC loop system is proposed to significantly influence information processing, for instance the ability to screen out, inhibit, filter, or gate extraneous stimuli and to direct selective attention to salient features of the environment. Failures of these attentional gating mechanisms might overload patients with the excessive processing of both sensory and cognitive stimuli, which could lead to a breakdown of cognitive integrity and difficulty in distinguishing self from non-self and failure to integrate an overwhelming flood of information. Descriptive elaboration of the mentioned effects can be found in the literature on schizophrenia as well as in descriptions of hallucinogenic drug action.

Despite strong evidence linking serotonin and psychosis, novel research indicates that some behavioral effects of drugs such as psilocybin appear to be independent of the classical 5-HT2A receptor-agonist actions, implying that the model described here is not the only underlying framework at play. Interdisciplinary research enterprises have set out to study the convergence of serotonergic and glutamatergic models of psychosis and dynamic neurotransmitter interactions, derived from the study of hallucinogenic drugs, in the future.

Synthetic surprise

Synthetic surprise is a theoretical concept explaining the altered states of consciousness induced by psychedelic substances like LSD and psilocybin. Central to this concept is the activation of the 5-HT2A receptor by psychedelics. The hypothesis suggests that these substances induce a state of synthetic surprise through the selective activation of the 5-HT receptors system, based on recent insights supporting a role of 5-HT in signaling surprise. This state aligns with the 'prediction error' in the predictive coding framework of brain function, where there's a discrepancy between the brain's expectations and the actual sensory input. The precision of this sensory data is crucial in modifying the brain's pre-existing beliefs or 'priors'. Under the influence of psychedelics, the interplay between top-down expectations and bottom-up sensory information is altered, leading to the characteristic changes in consciousness. Hallucinations in this context can be explained by the previously proposed "Strong priors" theory. This understanding of synthetic surprise has significant implications for the clinical use of psychedelic substances. The ability of psychedelics to induce surprise is proposed to be central to their therapeutic potential, especially in disrupting maladaptive cognitive and perceptual patterns.

Higher consciousness

From Wikipedia, the free encyclopedia

Philosophy

Fichte

Johann Gottlieb Fichte (1762–1814) was one of the founding figures of German idealism, which developed from the theoretical and ethical writings of Immanuel Kant. His philosophy forms a bridge between the ideas of Kant and those of the German idealist Georg Wilhelm Friedrich Hegel.

Fichte distinguished the finite or empirical ego from the pure or infinite ego. The activity of this "pure ego" can be discovered by a "higher intuition".

According to Michael Whiteman, Fichte's philosophical system "is a remarkable western formulation of eastern mystical teachings (of which he seems to have had no direct knowledge)."

Schopenhauer

In 1812, Arthur Schopenhauer started to use the term "the better consciousness", a consciousness that "lies beyond all experience and thus all reason, both theoretical and practical (instinct)."

According to Yasuo Kamata, Schopenhauer's idea of "the better consciousness" finds its origin in Fichte's idea of a "higher consciousness" (höheres Bewusstsein) or "higher intuition", and also bears resemblance to Schelling's notion of "intellectual intuition". According to Schopenhauer himself, his notion of a "better consciousness" was different from Schelling's notion of "intellectual intuition", since Schelling's notion required intellectual development of the understanding, while his notion of a "better consciousness" was "like a flash of insight, with no connection to the understanding."

According to Schopenhauer,

The better consciousness in me lifts me into a world where there is no longer personality and causality or subject or object. My hope and my belief is that this better (supersensible and extra-temporal) consciousness will become my only one, and for that reason I hope that it is not God. But if anyone wants to use the expression God symbolically for the better consciousness itself or for much that we are able to separate or name, so let it be, yet not among philosophers I would have thought.

Main types

Different types of higher states of consciousness can arise individually or in various combinations. The list of known types of higher states of consciousness:

  • modified states of consciousness, achieved with the help of meditative psychotechnics;
  • optimal experience and the “flow” state;
  • euphoria;
  • lucid dreaming;
  • out-of-body experience;
  • near-death experience;
  • mystical experience (sometimes regarded as the highest of all higher states of consciousness)

Religion

Schleiermacher

Friedrich Schleiermacher (1768–1834) made a distinction between lower and higher self-consciousness. In Schleirmacher's theology, self-consciousness contains "a feeling that points to the presence of an absolute other, God, as actively independent of the self and its 'world'." For Schleiermacher, "all particular manifestations of piety share a common essence, the sense of dependency on God as the outside 'infinite'." The feeling of dependency, or "God-consciousness", is a higher form of consciousness. This consciousness is not "God himself", since God would then no longer be "an infinite infinite, but a finite infinite, a mere projection of consciousness."

For Schleiermacher, the lower self-consciousness is "the animal part of mankind", which includes basic sensations such as hunger, thirst, pain and pleasure, as well as basic drives and pleasures, and higher self-consciousness is, in the words of theologian Dawn DeVries, "the part of the human being that is capable of transcending animal instincts", and the "point of contact with God". Bunge describes this as "the essence of being human".

When this consciousness is present, "people are not alienated from God by their instincts". The relation between the lower and the higher consciousness is akin to "Paul's struggle of the spirit to overcome the flesh", or the distinction between the natural and the spiritual side of human beings.

19th-century movements

The idea of a "wider self walled in by the habits of ego-consciousness" and the search for a "higher consciousness" was manifested in 19th century movements such as Theosophy, New Thought, Christian Science, and Transcendentalism.

The 19th-century Transcendentalists saw the entire physical world as a representation of a higher spiritual world. They believed that humans could elevate themselves above their animal instincts, attain a higher consciousness, and partake in this spiritual world.

Higher self is a term associated with multiple belief systems, but its basic premise describes an eternal, omniscient, conscious, and intelligent being, who is one's real self. Blavatsky, who founded the Theosophical Movement, formally defined the higher self as "Atma the inseparable ray of the Universe and one self. It is the God above, more than within, us". According to Blavatsky, each and every individual has a higher self. She wrote:

By that higher intuition acquired by Theosophia -- or God-knowledge, which carried the mind from the world of form into that of formless spirit, man has been sometimes enabled in every age and every country to perceive things in the interior or invisible world.

Blavatsky refers to Fichte in her explanation of Theosophy:

Theosophy ... prompted such men as Hegel, Fichte and Spinoza to take up the labors of the old Grecian philosophers and speculate upon the One Substance -- the Deity, the Divine All proceeding from the Divine Wisdom -- incomprehensible, unknown and unnamed.

20th-century movements

Aleister Crowley, founder of Thelema, referred to the higher consciousness or self as Harpocrates, which he identified as a name for the Holy Guardian Angel. In his early writings, Crowley states that the Holy Guardian Angel is the "silent self", the equivalent of the Genius of the Hermetic Order of the Golden Dawn, the Augoeides of Iamblichus, the Ātman of Hinduism, and the Daimon of the ancient Greeks.

Clairvoyant Edgar Cayce referred to higher consciousness as "the Christ pattern". This is not necessarily a tenet of Christianity, but the conviction that a regular person can be attuned to reach the same level of spirituality as did the historical Jesus.

Modern spirituality

The idea of "lower" and "higher" consciousness has gained popularity in modern popular spirituality. According to James Beverley, it lies at the heart of the New Age movement. Most New Age literature defines the Higher self as an extension of the self to a godlike state. This Higher Self is essentially an extension of the worldly self. With this perspective, New Age texts teach that the self creates its own reality when in union with the Higher Self.

Integral theorist Ken Wilber has tried to integrate eastern and western models of the mind, using the notion of "lower" and "higher" consciousness. In his book The Spectrum of Consciousness Wilber describes consciousness as a spectrum with ordinary awareness at one end, and more profound types of awareness at higher levels. In later works he describes the development of consciousness as a development from lower consciousness, through personal consciousness, to higher transpersonal consciousness.

Cognitive science

Gerald Edelman distinguishes higher consciousness or "secondary consciousness" from "primary consciousness", defined as simple awareness that includes perception and emotion. Higher consciousness in contrast, "involves the ability to be conscious of being conscious", and "allows the recognition by a thinking subject of his or her own acts and affections". Higher consciousness requires, at a minimal level semantic ability, and "in its most developed form, requires linguistic ability, or the mastery of a whole system of symbols and a grammar".

Psychotropics

Psychedelic drugs can be used to alter the brain cognition and perception, some believing this to be a state of higher consciousness and transcendence. Typical psychedelic drugs are hallucinogens including LSD, DMT, cannabis, peyote, and psilocybin mushrooms. According to Wolfson, these drug-induced altered states of consciousness may result in a more long-term and positive transformation of self.

According to Dutta, psychedelic drugs may be used for psychoanalytic therapy, as a means to gain access to the higher consciousness, thereby providing patients the ability to access memories that are held deep within their mind.

Public key infrastructure

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