Anesthesia awareness, also referred to as accidental awareness during general anaesthesia (AAGA) or unintended intra-operative awareness, is a potential complication occurring during general anesthesia where the intended state of complete unconsciousness is not maintained throughout the whole procedure. It can occur either because of failure to deliver sufficient anesthetic medication to the patient's body, or because of individual patient factors that mean the patient is resistant to what would normally be an adequate dose of anesthetic medication.

There are two states of consciousness that may be present:

- Awareness: That is, patients seem to be cognizant responding to commands but with no postoperative recall or memory of the events.

- Awareness and recall: That is, patients can recall events postoperatively, but were not necessarily conscious enough to respond to commands.

The incidence of a state with both responses in diverse degrees is also possible. The drugs that induce paralysis would also prevent responding to commands.

Like coma, chronic coma results mostly from cortical or white-matter damage after neuronal or axonal injury, or from focal brainstem lesions.Usually the metabolism in the grey matter decreases to 50-70% of the normal range. The patient lacks awareness and arousal. The patient lies with eyes closed and is not aware of self or surroundings. Stimulation cannot produce spontaneous periods of wakefulness and eye-opening, unlike patients in vegetative state. In medicine, a coma (from the Greek κῶμα koma, meaning deep sleep) is a state of unconsciousness, lasting more than six hours in which a person cannot be awakened, fails to respond normally to painful stimuli, light, sound, lacks a normal sleep-wake cycle and does not initiate voluntary actions. Although, according to the Glasgow Coma Scale, a person with confusion is considered to be in the mildest coma. But cerebral metabolism has been shown to correlate poorly with the level of consciousness in patients with mild to severe injury within the first month after traumatic brain injury (TBI).

A person in a state of coma is described as comatose. In general patients surviving a coma recover gradually within 2–4 weeks. But recovery to full awareness and arousal is not always possible. Some patients do not progress further than vegetative state or minimally conscious state and sometimes this also results in prolonged stages before further recovery to complete consciousness.

Although a coma patient may appear to be awake, they are unable to consciously feel, speak, hear, or move. For a patient to maintain consciousness, two important neurological components must function impeccably. The first is the cerebral cortex which is the gray matter covering the outer layer of the brain. The other is a structure located in the brainstem, called reticular activating system (RAS or ARAS). Injury to either or both of these components is sufficient to cause a patient to experience a coma.

In locked-in syndrome the patient has awareness, sleep-wake cycles, and meaningful behavior (viz., eye-movement), but is isolated due to quadriplegia and pseudobulbar palsy, resulting from the disruption of corticospinal and corticobulbar pathways. Locked-in syndrome is a condition in which a patient is aware and awake but cannot move or communicate verbally due to complete paralysis of nearly all voluntary muscles in the body except for the eyes. Eye or eyelid movements are the main method of communication. Total locked-in syndrome is a version of locked-in syndrome where the eyes are paralyzed as well.

A minimally conscious state (MCS) is a disorder of consciousness distinct from persistent vegetative state and locked-in syndrome. Unlike persistent vegetative state, patients with MCS have partial preservation of conscious awareness. MCS is a relatively new category of disorders of consciousness. The natural history and longer term outcome of MCS have not yet been thoroughly studied. The prevalence of MCS was estimated to be 112,000 to 280,000 adult and pediatric cases.

Most PVS patients are unresponsive to external stimuli and their conditions are associated with different levels of consciousness. Some level of consciousness means a person can still respond, in varying degrees, to stimulation. A person in a coma, however, cannot. In addition, PVS patients often open their eyes in response to feeding, which has to be done by others; they are capable of swallowing, whereas patients in a coma subsist with their eyes closed (Emmett, 1989).

PVS patients' eyes might be in a relatively fixed position, or track moving objects, or move in a "disconjugate" (i.e., completely unsynchronized) manner. They may experience sleep-wake cycles, or be in a state of chronic wakefulness. They may exhibit some behaviors that can be construed as arising from partial consciousness, such as grinding their teeth, swallowing, smiling, shedding tears, grunting, moaning, or screaming without any apparent external stimulus.

Individuals in PVS are seldom on any life-sustaining equipment other than a feeding tube because the brainstem, the center of vegetative functions (such as heart rate and rhythm, respiration, and gastrointestinal activity) is relatively intact (Emmett, 1989).

Many people emerge spontaneously from a vegetative state within a few weeks. The chances of recovery depend on the extent of injury to the brain and the patient's age – younger patients having a better chance of recovery than older patients. A 1994 report found that of those who were in a vegetative state a month after a trauma, 54% had regained consciousness by a year after the trauma, whereas 28% had died and 18% were still in the vegetative state. But for non-traumatic injuries such as strokes, only 14% had recovered consciousness at one year, 47% had died, and 39% were still vegetative. Patients who were vegetative six months after the initial event were much less likely to have recovered consciousness a year after the event than in the case of those who were simply reported vegetative at one month. A "New Scientist" article from 2000 gives a pair of graphs showing changes of patient status during the first 12 months after head injury and after incidents depriving the brain of oxygen. After a year, the chances that a PVS patient will regain consciousness are very low and most patients who do recover consciousness experience significant disability. The longer a patient is in a PVS, the more severe the resulting disabilities are likely to be. Rehabilitation can contribute to recovery, but many patients never progress to the point of being able to take care of themselves.

There are two dimensions of recovery from a persistent vegetative state: recovery of consciousness and recovery of function. Recovery of consciousness can be verified by reliable evidence of awareness of self and the environment, consistent voluntary behavioral responses to visual and auditory stimuli, and interaction with others. Recovery of function is characterized by communication, the ability to learn and to perform adaptive tasks, mobility, self-care, and participation in recreational or vocational activities. Recovery of consciousness may occur without functional recovery, but functional recovery cannot occur without recovery of consciousness (Ashwal, 1994).

Dejerine–Roussy syndrome is most commonly preceded by numbness in the affected side. In these cases, numbness is replaced by burning and tingling sensations, widely varying in degree of severity across all cases. The majority of those reported are cases in which the symptoms are severe and debilitating. Burning and tingling can also be accompanied by hypersensitivity, usually in the form of dysaesthesia or allodynia. Less commonly, some patients develop severe ongoing pain with little or no stimuli.

Allodynia is pain from a stimulus that would normally not cause pain. For example, there is a patient who experiences unrelenting pain when a breeze touches his skin. Most patients experiencing allodynia, experience pain with touch and pressure, however some can be hypersensitive to temperature.

Dysaesthesia is defined as pain due to thalamic lesioning. This form of neuropathic pain can be any combination of itching, tingling, burning, or searing experienced spontaneously or from stimuli.

Allodynia and dysaesthesia replace numbness between one week and a few months after a thalamic stroke. In general, once the development of pain has stopped, the type and severity of pain will be unchanging and if untreated, persist throughout life. Consequentially, many will undergo some form of pain treatment and adjust to their new lives as best they can.

Pain associated with Dejerine–Roussy syndrome is sometimes coupled with anosognosia or somatoparaphrenia which causes a patient having undergone a right-parietal, or right-sided stroke to deny any paralysis of the left side when indeed there is, or deny the paralyzed limb(s) belong to them. Although debatable, these symptoms are rare and considered part of a "thalamic phenomenon", and are not normally considered a characteristic of Dejerine–Roussy syndrome.

Minimally conscious state (MCS) is defined as a condition of severely altered consciousness in which minimal but definite behavioral evidence of self or environmental awareness is demonstrated.

Postoperative cognitive dysfunction (POCD) is a decline in cognitive function (especially in memory and executive functions) that may last from a few days to a few weeks after surgery. In rare cases, this disorder may persist for several months after major surgery. POCD is distinct from emergence delirium. It occurs most commonly in older patients and those with pre-existing cognitive impairment.

The causes of POCD are not understood. It does not appear to be caused by lack of oxygen or impaired blood flow to the brain and is equally likely under regional and general anesthesia. It may be mediated by the body's inflammatory response to surgery.

Experiences - are characterized by the presence of the following three factors:

- disembodiment, an apparent location of the self outside one's body;

- impression of seeing the world from an elevated and distanced visuo-spatial perspective or extracorporeal, but egocentric visuo-spatial perspective;

- impression of seeing one's own body from this perspective (autoscopy).

Laboratory of Cognitive Neuroscience, École Polytechnique Fédérale de Lausanne, Lausanne, and Department of Neurology, University Hospital, Geneva, Switzerland, have reviewed some of the classical precipitating factors of autoscopy. These are sleep, drug abuse, and general anesthesia as well as neurobiology. They have compared them with recent findings on neurological and neurocognitive mechanisms of the autoscopy. The reviewed data suggest that autoscopic experiences are due to functional disintegration of lower-level multisensory processing and abnormal higher-level self-processing at the temporoparietal junction.

Autoscopy is the experience in which an individual perceives the surrounding environment from a different perspective, from a position outside of his or her own body. Autoscopy comes from the ancient Greek ("self") and ("watcher").

Autoscopy has been of interest to humankind from time immemorial and is abundant in the folklore, mythology, and spiritual narratives of most ancient and modern societies. Cases of autoscopy are commonly encountered in modern psychiatric practice. According to neurological research, autoscopic experiences are hallucinations.

Anaphia, also known as tactile anesthesia, is a medical symptom in which there is a total or partial absence of the sense of touch.

Anaphia is a common symptom of spinal cord injury and neuropathy.

Somatoparaphrenia is a type of monothematic delusion where one denies ownership of a limb or an entire side of one's body. Even if provided with undeniable proof that the limb belongs to and is attached to their own body, the patient produces elaborate confabulations about whose limb it really is, or how the limb ended up on their body. In some cases, delusions become so elaborate that a limb may be treated and cared for as if it were a separate being.

Somatoparaphrenia differs from a similar disorder, asomatognosia, which is characterized as loss of recognition of half of the body or a limb, possibly due to paralysis or unilateral neglect. For example, asomatognosic patients may mistake their arm for the doctor's. However, they can be shown their limb and this error is temporarily corrected.

Somatoparaphrenia has been reported to occur predominately in the left arm of one's body, and it is often accompanied by left-sided paralysis and anosognosia (denial or lack of awareness) of the paralysis. The link between somatoparaphrenia and paralysis has been documented in many clinical cases and while the question arises as to whether paralysis is necessary for somatoparaphrenia to occur, anosognosia is not, as documented by cases with somatoparaphrenia and paralysis with no anosognosia.

Dejerine-Roussy is a rare pain syndrome. Individuals with emerging Dejerine–Roussy syndrome usually report they are experiencing unusual pain or sensitivity that can be allodynic in nature or triggered by seemingly unrelated stimuli (sounds, tastes). Symptoms are typically lateralized and may include vision loss or loss of balance (position sense). Workup should be performed by a neurologist and brain imaging to look for evidence of infarction or tumor should be obtained.

Tardive Dysmentia is a rarely used term introduced in a 1983 paper to describe "changes in affect, activation level, and interpersonal interaction", and hypothesized to be caused by long-term exposure to neuroleptic drugs in the same way as the much better known syndrome of tardive dyskinesia. Several papers in the following years discussed the validity of the concept, and this small literature was reviewed in a 1993 publication by M. S. Myslobodsky, who drew attention to the "possibility that the syndrome of dysmentia is occasional excessive emotional reactivity, enhanced responsiveness to environmental stimuli, and indifference to or reduced awareness of the patient's abnormal involuntary movements", but concluded that the pathophysiology is uncertain. Since then, the term has fallen into disuse, receiving at most only passing mentions in the literature.

Asomatognosia is a neurological disorder characterized as loss of recognition or awareness of part of the body. The failure to acknowledge, for example, a limb, may be expressed verbally or as a pattern of neglect. The limb may also be attributed to another person, a delusion known as somatoparaphrenia. However, they can be shown their limb and this error is temporarily corrected. Some authors have focused on the prevalence of hemispatial neglect in such patients.

POCD is common after cardiac surgery, and recent studies have now verified that POCD also exists after major non-cardiac surgery, although at a lower incidence. The risk of POCD increases with age, and the type of surgery is also important because there is a very low incidence associated with minor surgery. POCD is common in adult patients of all ages at hospital discharge after major noncardiac surgery, but only the elderly (aged 60 years or older) are at significant risk for long-term cognitive problems. Patients with POCD are at an increased risk of death in the first year after surgery. Research interest has increased since early 2000, especially as more elderly patients are able to undergo successful minor and major surgeries.

POCD has been studied through various institutions since the inception of the IPOCDS-I study centred in Eindhoven, Netherlands and Copenhagen, Denmark. This study found no causal relationship between cerebral hypoxia and low blood pressure and POCD. Age, duration of anaesthesia, introperative complications, and postoperative infections were found to be associated with POCD.

- POCD is just as likely to occur after operations under regional anesthesia as under general anesthesia.

- More likely after major operations than minor operations.

- More likely after heart operations than other types of surgery.

- More likely in aged than in younger patients.

- More likely in older patients with high alcohol intake/abuse.

- People with higher preoperative ASA physical status scores are more likely to develop POCD.

- People with lower educational level are more likely to develop POCD than those with a higher educational level.

- People with prior history of a stroke, even though there is complete functional recovery, are more likely to develop POCD.

- More likely in the elderly with pre-existing declining mental functions, termed mild cognitive impairment (MCI). MCI is a transitional zone between normal mental function and evident Alzheimer's disease or other forms of dementia. It is insidious, and seldom recognized, except in retrospect after affected persons are evidently demented.

- Delirium and severe worsening of mental function is very likely in those with clinically evident Alzheimer's disease or other forms of dementia, as well as those with a history of delirium after previous operations.

It has been suggested that damage to the posterior cerebral regions (temporoparietal junction) of the cortex may play a significant role in the development of somatoparaphrenia. However, more recent studies have shown that damage to deep cortical regions such as the posterior insula and subcortical structures such as the basal ganglia, the thalamus and the white matter connecting the thalamus to the cortex may also play a significant role in the development of somatoparaphrenia. It has also been suggested that involvement of deep cortical and subcortical grey structures of the temporal lobe may contribute to reduce the sense of familiarity experienced by somatoparaphrenic patients for their paralyzed limb.

Postoperative residual curarization (PORC) is a residual paresis after emergence from general anesthesia with neuromuscular-blocking drugs.

Postanesthetic shivering (PAS) is shivering after anesthesia.

The intensity of PAS may be graded using the scale described by Crossley and Mahajan:

Postanesthetic shivering is one of the leading causes of discomfort in patients recovering from general anesthesia. It usually results due to the anesthetic inhibiting the body's thermoregulatory capability, although cutaneous vasodilation (triggered by post-operative pain) may also be a causative factor. First-line treatment consists of warming the patient; more persistent/severe cases may be treated with medications such as tramadol, pethidine, clonidine and nefopam, which work by reducing the shivering threshold temperature and reducing the patient's level of discomfort. As these medications may react and/or synergize with the anesthetic agents employed during the surgery, their use is generally avoided when possible.

Hypokalemic sensory overstimulation is characterized by a subjective experience of sensory overload and a relative resistance to lidocaine local anesthesia. The sensory overload is treatable with oral potassium gluconate. The phenotype overlaps with that of attention deficit disorder, raising the possibility of subtypes of attention deficit disorder that have a peripheral sensory cause and possible new forms of therapy.

Hypokalemic sensory overstimulation is a term coined by MM Segal to describe a syndrome that has been reported in a single case-study by his group. Segal describes the syndrome as a form of neurological disorder that has similarities to attention deficit hyperactivity disorder and has several similarities to disorders of ion channels, in particular to the muscle disorder hypokalemic periodic paralysis.

It is medically related to disorders of ion channels, in particular to the muscle disorder hypokalemic periodic paralysis and is similar in nature to ADHD, as the prominent feature of hypokalemic sensory overstimulation is the feeling of sensory overstimulation that is also characteristic of attention deficit disorder and the over stimulation of the nervous system.. It may also be connected with premenstrual syndrome and the body's natural sodium levels.

Although largely used to describe unawareness of impairment after brain injury or stroke, the term 'anosognosia' is occasionally used to describe the lack of insight shown by some people with anorexia nervosa. They do not seem to recognize that they have a mental illness. There is evidence that 'anosognosia' related to schizophrenia may be the result of frontal lobe damage. E. Fuller Torrey, a psychiatrist and schizophrenia researcher, has stated that among those with schizophrenia and bipolar disorder, anosognosia is the most prevalent reason for not taking medications.

Riddoch syndrome (also known as the "Riddoch phenomenon") is an ocular affectation often caused by lesions in the occipital lobe which limit the sufferer's ability to distinguish objects. Only moving objects in a blind field are visible, static ones being invisible to the patient. The moving objects are not perceived to have color or detail. The subject may only have awareness of the movement without visual perception of it (gnosanopsia), or the general shape of a moving object may be perceivable as a shadow like outline.

At least one patient was able to use a rocking chair—putting non-moving surroundings in relative motion to her head—to improve her motion perception. She eventually was able to do the same with just voluntary movement of her head.