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.

A persistent vegetative state (PVS) is a disorder of consciousness in which patients with severe brain damage are in a state of partial arousal rather than true awareness. After four weeks in a vegetative state (VS), the patient is classified as in a persistent vegetative state. This diagnosis is classified as a "permanent vegetative state" some months (3 in the US and 6 in the UK) after a non-traumatic brain injury or one year after a traumatic injury. Nowadays, more doctors and neuroscientists prefer to call the state of consciousness an "unresponsive wakefulness syndrome", primarily because of ethical questions about whether a patient can be called "vegetative" or not.

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).

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.

Locked-in syndrome usually results from quadriplegia and the inability to speak in otherwise cognitively intact individuals. Those with locked-in syndrome may be able to communicate with others through coded messages by blinking or moving their eyes, which are often not affected by the paralysis. The symptoms are similar to those of sleep paralysis. Patients who have locked-in syndrome are conscious and aware, with no loss of cognitive function. They can sometimes retain proprioception and sensation throughout their bodies. Some patients may have the ability to move certain facial muscles, and most often some or all of the extraocular muscles. Individuals with the syndrome lack coordination between breathing and voice. This prevents them producing voluntary sounds, though the vocal cords are not paralysed.

The signs of vertiginous epilepsy often occur without a change in the subject’s consciousness so that they are still aware while experiencing the symptoms. It is often described as a sudden onset of feeling like one is turning in one direction, typically lasting several seconds. Although subjects are aware during an episode, they often cannot remember specific details due to disorientation, discomfort, and/or partial cognitive impairment. This sensation of rotational movement in the visual and auditory planes is also known as a vertiginous aura (symptom), which can precede a seizure or may constitute a seizure itself. Auras are a “portion of the seizure that occur before consciousness is lost and for which memory is retained afterwards.” Auras can be focused in different regions of the brain and can thus affect different functions. Some such symptoms that may accompany vertiginous epilepsy include:

- Auditory hallucination

- Cognitive impairment

- Motor activity

- Ictal behavior

- Limbic auras

Many people tend to mistake dizziness as vertigo, and although they sound similar, dizziness is not considered a symptom of vertiginous epilepsy. Dizziness is the sensation of imbalance or floating, impending loss of consciousness, and/or confusion. This is different from vertigo which is characterized by the illusion of rotational movement caused by the “conflict between the signals sent to the brain by balance- and position-sensing systems of the body”.

TBI patients may have sensory problems, especially problems with vision; they may not be able to register what they are seeing or may be slow to recognize objects. Also, TBI patients often have difficulty with hand–eye coordination, causing them to seem clumsy or unsteady. Other sensory deficits include problems with hearing, smell, taste, or touch. Tinnitus, a ringing or roaring in the ears, may occur. A person with damage to the part of the brain that processes taste or smell may perceive a persistent bitter taste or noxious smell. Damage to the part of the brain that controls the sense of touch may cause a TBI patient to develop persistent skin tingling, itching, or pain. These conditions are rare and difficult to treat.

The most prominent symptom of post-traumatic amnesia (PTA) is a loss of memory of the present time. As a result, patients are often unaware of their condition and may behave as if they are going about their regular lives. This can cause complications if patients are confined to a hospital and may lead to agitation, distress and/or anxiety. Many patients report feeling as though they were being "held prisoner" and being prevented from carrying on with their daily lives. Other symptoms include agitation, confusion, disorientation, and restlessness.

Patients also often display behavioral disturbances. Patients may shout, swear and behave in a disinhibited fashion. There have been cases in which patients who do not recognize anyone will ask for family members or acquaintances that they have not seen in years. Some patients exhibit childlike behavior. Other patients show uncharacteristically quiet, friendly and loving behavior. Although this behavior may seem less threatening because of its lack of aggressiveness, it may be equally worrisome.

PTA patients are often unaware of their surroundings and will ask questions repeatedly. Patients may also have a tendency to wander off, which can be a major concern in those who have suffered additional injuries at the time of trauma, such as injured limbs, as it may lead to the worsening of these secondary injuries.

Locked-in syndrome (LIS), also known as pseudocoma, is a condition in which a patient is aware but cannot move or communicate verbally due to complete paralysis of nearly all voluntary muscles in the body except for vertical eye movements and blinking. The individual is conscious and sufficiently intact cognitively to be able to communicate with eye movements.

The EEG is "normal" in locked-in syndrome.

Total locked-in syndrome, or completely locked-in state (CLIS), is a version of locked-in syndrome wherein the eyes are paralyzed as well. Fred Plum and Jerome Posner coined the term for this disorder in 1966.

Seizures are purely occipital and primarily manifest with elementary visual hallucinations, blindness or both.

They are usually frequent and diurnal, develop rapidly within seconds and are brief, lasting from a few seconds to 1–3 min, and, rarely, longer.

Elementary visual hallucinations are the most common and characteristic ictal symptoms, and are most likely to be the first and often the only clinical manifestation. They consist mainly of small multicoloured circular patterns that often appear in the periphery of a visual field, becoming larger and multiplying during the course of the seizure, frequently moving horizontally towards the other side.

Other occipital symptoms, such as sensory illusions of ocular movements and ocular pain, tonic deviation of the eyes, eyelid fluttering or repetitive eye closures, may occur at the onset of the seizures or appear after the elementary visual hallucinations. "Deviation of the eyes", often associated with ipsilateral turning of the head, is the most common (in about 70% of cases) nonvisual ictal symptom. It is often associated with ipsilateral turning of the head and usually starts after visual hallucinations, although it may also occur while the hallucinations still persist. It may be mild, but more often it is severe and progresses to hemiconvulsions and secondarily generalised tonic clonic seizures (GTCS). Some children may have seizures of eye deviation from the start without visual hallucinations.

"Forced eyelid closure and eyelid blinking" occur in about 10% of patients, usually at a stage at which consciousness is impaired. They signal an impending secondarily GTCS.

"Ictal blindness", appearing from the start or, less commonly, after other manifestations of occipital seizures, usually lasts for 3–5 min. It can occur alone and be the only ictal event in patients who could, at other times, have visual hallucinations without blindness.

Complex visual hallucinations, visual illusions and other symptoms resulting from more anterior ictal spreading rarely occur from the start. They may terminate in hemiconvulsions or generalised convulsions.

Ictal headache, or mainly orbital pain, may occur and often precedes visual or other ictal occipital symptoms in a small number of patients.

Consciousness is not impaired during the visual symptoms (simple focal seizures), but may be disturbed or lost in the course of the seizure, usually before eye deviation or convulsions.

Occipital seizures of ICOE-G may rarely progress to extra-occipital manifestations, such as hemiparaesthesia. Spread to produce symptoms of temporal lobe involvement is exceptional and may indicate a symptomatic cause.

Post-ictal headache, mainly diffuse, but also severe, unilateral and pulsating, or indistinguishable from migraine headache, occurs in half the patients, in 10% of whom it may be associated with nausea and vomiting.

Circadian distribution: Visual seizures are predominantly diurnal and can occur at any time of the day. Longer seizures, with or without hemi or generalised convulsions, tend to occur either during sleep, causing the patient to wake up, or after awakening. Thus, some children may have numerous diurnal visual seizures and only a few seizures that are exclusively nocturnal or occur on awakening.

Frequency of seizures: If untreated, patients experience frequent and brief visual seizures (often several every day or weekly). However, propagation to other seizure manifestations, such as focal or generalised convulsions, is much less frequent.

Vertiginous epilepsy is infrequently the first symptom of a seizure, characterized by a feeling of vertigo. When it occurs there is a sensation of rotation or movement that lasts for a few seconds before full seizure activity. While the specific causes of this disease are speculative there are several methods for diagnosis, the most important being the patient's recall of episodes. Most times, those diagnosed with vertiginous seizures are left to self-manage their symptoms or are able to use anti-epileptic medication to dampen the severity of their symptoms. Vertiginous epilepsy has also been referred to as Epileptic vertigo, Vestibular epilepsy, Vestibular seizures, and Vestibulogenic seizures in different cases, but vertiginous epilepsy is the preferred term.

TBI may cause emotional or behavioral problems and changes in personality. Emotional symptoms that can follow TBI include emotional instability, depression, anxiety, hypomania, mania, apathy, irritability, and anger. TBI appears to predispose a person to psychiatric disorders including obsessive compulsive disorder, alcohol or substance abuse or substance dependence, dysthymia, clinical depression, bipolar disorder, phobias, panic disorder, and schizophrenia. About one quarter of people with TBI suffer from clinical depression, and about 9% suffer mania. The prevalence of all psychiatric illnesses is 49% in moderate to severe TBI and 34% in mild TBI within a year of injury, compared with 18% of controls. People with TBI continue to be at greater risk for psychiatric problems than others even years after an injury. Problems that may persist for up to two years after the injury include irritability, suicidal ideation, insomnia, and loss of the ability to experience pleasure from previously enjoyable experiences.

Behavioral symptoms that can follow TBI include disinhibition, inability to control anger, impulsiveness, lack of initiative, inappropriate sexual activity, and changes in personality. Different behavioral problems are characteristic of the location of injury; for instance, frontal lobe injuries often result in disinhibition and inappropriate or childish behavior, and temporal lobe injuries often cause irritability and aggression.

Neurological disorders can be categorized according to the primary location affected, the primary type of dysfunction involved, or the primary type of cause. The broadest division is between central nervous system disorders and peripheral nervous system disorders. The Merck Manual lists brain, spinal cord and nerve disorders in the following overlapping categories:

- Brain:

- Brain damage according to cerebral lobe "(see also 'lower' brain areas such as basal ganglia, cerebellum, brainstem)":

- Frontal lobe damage

- Parietal lobe damage

- Temporal lobe damage

- Occipital lobe damage

- Brain dysfunction according to type:

- Aphasia (language)

- Dysgraphia (writing)

- Dysarthria (speech)

- Apraxia (patterns or sequences of movements)

- Agnosia (identifying things or people)

- Amnesia (memory)

- Spinal cord disorders (see spinal pathology, injury, inflammation)

- Peripheral neuropathy and other Peripheral nervous system disorders

- Cranial nerve disorder such as Trigeminal neuralgia

- Autonomic nervous system disorders such as dysautonomia, Multiple System Atrophy

- Seizure disorders such as epilepsy

- Movement disorders of the central and peripheral nervous system such as Parkinson's disease, Essential tremor, Amyotrophic lateral sclerosis, Tourette's Syndrome, Multiple Sclerosis and various types of Peripheral Neuropathy

- Sleep disorders such as Narcolepsy

- Migraines and other types of Headache such as Cluster Headache and Tension Headache

- Lower back and neck pain (see Back pain)

- Central neuropathy (see Neuropathic pain)

- Neuropsychiatric illnesses (diseases and/or disorders with psychiatric features associated with known nervous system injury, underdevelopment, biochemical, anatomical, or electrical malfunction, and/or disease pathology e.g. Attention deficit hyperactivity disorder, Autism, Tourette's syndrome and some cases of obsessive compulsive disorder as well as the neurobehavioral associated symptoms of degeneratives of the nervous system such as Parkinson's disease, essential tremor, Huntington's disease, Alzheimer's disease, multiple sclerosis and organic psychosis.)

Many of the diseases and disorders listed above have neurosurgical treatments available (e.g. Tourette's Syndrome, Parkinson's disease, Essential tremor and Obsessive compulsive disorder).

- Delirium and dementia such as Alzheimer's disease

- Dizziness and vertigo

- Stupor and coma

- Head injury

- Stroke (CVA, cerebrovascular attack)

- Tumors of the nervous system (e.g. cancer)

- Multiple sclerosis and other demyelinating diseases

- Infections of the brain or spinal cord (including meningitis)

- Prion diseases (a type of infectious agent)

- Complex regional pain syndrome (a chronic pain condition)

Neurological disorders in non-human animals are treated by veterinarians.

In the UK, the formal rules for the diagnosis of brainstem death have undergone only minor modifications since they were first published in 1976. The most recent revision of the UK's Department of Health Code of Practice governing use of that procedure for the diagnosis of death reaffirms the preconditions for its consideration. These are:

1. There should be no doubt that the patient’s condition – deeply comatose, unresponsive and requiring artificial ventilation—is due to irreversible brain damage of known cause.

2. There should be no evidence that this state is due to depressant drugs.

3. Primary hypothermia as the cause of unconsciousness must have been excluded, and

4. Potentially reversible circulatory, metabolic and endocrine disturbances likewise.

5. Potentially reversible causes of apnoea (dependence on the ventilator), such as muscle relaxants and cervical cord injury, must be excluded.

With these pre-conditions satisfied, the definitive criteria are:

1. Fixed pupils which do not respond to sharp changes in the intensity of incident light.

2. No corneal reflex.

3. Absent oculovestibular reflexes – no eye movements following the slow injection of at least 50ml of ice-cold water into each ear in turn (the caloric reflex test).

4. No response to supraorbital pressure.

5. No cough reflex to bronchial stimulation or gagging response to pharyngeal stimulation.

6. No observed respiratory effort in response to disconnection of the ventilator for long enough (typically 5 minutes) to ensure elevation of the arterial partial pressure of carbon dioxide to at least 6.0 kPa (6.5 kPa in patients with chronic carbon dioxide retention). Adequate oxygenation is ensured by pre-oxygenation and diffusion oxygenation during the disconnection (so the brainstem respiratory centre is not challenged by the ultimate, anoxic, drive stimulus). This test—the apnoea test—is dangerous – and may prove lethal.

Two doctors, of specified status and experience, are required to act together to diagnose death on these criteria and the tests must be repeated after “a short period of time ... to allow return of the patient’s arterial blood gases and baseline parameters to the pre-test state”. These criteria for the diagnosis of death are not applicable to infants below the age of two months.

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.

The severity of post-traumatic amnesia (PTA) is directly related to its duration, although a longer duration does not necessarily indicate more severe symptoms. The duration of PTA in brain-injured patients is a useful predictor of the expected long-term effects of the injury, along with the duration of loss of consciousness(LOC), and scores on the Glasgow Coma Scale (GCS), which measures degrees of consciousness, with higher scores indicating higher levels of functioning. A score of 3 indicates complete unconsciousness, and a score of 15 indicates normal functioning.

In patients experiencing PTA for the duration of:

Up to 1 hour – The injury is very mild in severity and full recovery is expected. The patient may experience a few minor post-concussive symptoms (e.g. headaches, dizziness).

1 – 24 hours – The injury is moderate in severity and full recovery is expected. The patient may experience some minor post-concussive symptoms (e.g. headaches, dizziness).

1 – 7 days – The injury is severe, and recovery may take weeks to months. The patient may be able to return to work, but may be less capable than before the injury.

1 – 2 weeks – The injury is very severe, and recovery is likely to take many months. The patient is likely to experience long-lasting cognitive effects such as decreased verbal and non-verbal intelligence as well as decreased performance on visual tests. Patients should, however, still be able to return to work.

2 – 12 weeks – The injury is very severe, and recovery is likely to take a year or more. The patient is likely to exhibit permanent deficits in memory and cognitive function, and the patient is unlikely to be able to return to work.

12+ weeks – injury is very severe and accompanied by significant disabilities that will require long-term rehabilitation and management. The patient is unlikely to be able to return to work.

Note: return to work is meant to indicate a return to a reasonable level of functionality, both in professional and personal arenas.

The long-term prognosis of PTA is generally positive. Many patients do recover a great deal of cognitive function, although they may not return to their pre-injury state.

Idiopathic childhood occipital epilepsy of Gastaut (ICOE-G) is a pure but rare form of idiopathic occipital epilepsy that affects otherwise normal children and adolescents. It is classified amongst benign idiopathic childhood focal epilepsies such as rolandic epilepsy and Panayiotopoulos syndrome.

Focal aware seizures are seizures which affect only a small region of the brain, often the temporal lobes or structures found there such as the hippocampi. People who have focal aware seizures remain conscious. Focal aware seizures often precede larger focal impaired awareness seizures, where the abnormal electrical activity spreads to a larger area of the brain. This can result in a tonic-clonic seizure.

- Presentation

Focal onset aware seizures are a very subjective experience, and the symptoms vary greatly between people. This is due to the varying locations of the brain the seizures originate in e.g.: Rolandic. A focal aware seizure may go unnoticed by others or shrugged off by the sufferer as merely a "funny turn." Focal aware seizures usually start suddenly and are very brief, typically lasting 60 to 120 seconds.

Some common symptoms of a focal onset aware seizure, when the person is awake, are:

- preserved consciousness

- sudden and inexplicable feelings of fear, anger, sadness, happiness or nausea

- sensations of falling or movement

- experiencing of unusual feelings or sensations

- altered sense of hearing, smelling, tasting, seeing, and tactile perception (sensory illusions or hallucinations), or feeling as though the environment is not real (derealization) or dissociation from the environment or self (depersonalization)

- a sense of spatial distortion—things close by may appear to be at a distance

- déjà vu (familiarity) or jamais vu (unfamiliarity)

- laboured speech or inability to speak at all

- usually the event is remembered in detail

When the seizure occurs during sleep, the person will often become semi-conscious and act out a dream they were having while engaging with the real environment as normal. Objects and people usually appear normal or only slightly distorted to them, and will be able to communicate with them on an otherwise normal level.

However, since the person is still acting in the dream-like state from which they woke, they will assimilate any hallucinations or delusions into their communication, often speaking to a hallucinatory person or speaking of events or thoughts normally pertaining to the dream they were having or other hallucination.

While asleep symptoms include:

- onset usually in REM sleep

- dream like state

- appearance of full consciousness

- hallucinations or delusions

- behavior or visions typical in dreams

- ability to engage with the environment and other people as in full consciousness, though often behaving abnormally, erratically, or failing to be coherent

- complete amnesia or assimilating the memory as though it was a normal dream on regaining full consciousness

Although hallucinations may occur during focal aware seizures they are differentiated from psychotic symptoms by the fact that the person is usually aware that the hallucinations are not real.

- Jacksonian march

Jacksonian march or Jacksonian seizure is a phenomenon where a focal aware seizure spreads from the distal part of the limb toward the face (on same side of body). They involve a progression of the location of the seizure in the brain, which leads to a "march" of the motor presentation of symptoms.

Jacksonian seizures are initiated with abnormal electrical activity within the primary motor cortex. They are unique in that they travel through the primary motor cortex in succession, affecting the corresponding muscles, often beginning with the fingers. This is felt as a tingling sensation, or a feeling of waves through the fingers when touched together. It then affects the hand and moves on to more proximal areas on the same side of body. Symptoms often associated with a Jacksonian seizure are sudden head and eye movements, tingling, numbness, smacking of the lips, and sudden muscle contractions. Most of the time any one of these actions can be seen as normal movements, without being associated with the seizure occurring. They occur at no particular moment and last only briefly. They may result in secondary generalized seizure involving both hemispheres. They can also start at the feet, manifesting as tingling or pins and needles, and there are painful cramps in the foot muscles, due to the signals from the brain. Because it is a partial seizure, the postictal state is of normal consciousness .

Brainstem death is a clinical syndrome defined by the absence of reflexes with pathways through the brainstem—the “stalk” of the brain, which connects the spinal cord to the mid-brain, cerebellum and cerebral hemispheres—in a deeply comatose, ventilator-dependent patient.

Identification of this state carries a very grave prognosis for survival; cessation of heartbeat often occurs within a few days although it may continue for weeks or even months if intensive support is maintained.

In the United Kingdom, the formal diagnosis of brainstem death by the procedure laid down in the official Code of Practice permits the diagnosis and certification of death on the premise that a person is dead when consciousness and the ability to breathe are permanently lost, regardless of continuing life in the body and parts of the brain, and that death of the brainstem alone is sufficient to produce this state.

This concept of brainstem death is also accepted as grounds for pronouncing death for legal purposes in India and Trinidad & Tobago. Elsewhere in the world the concept upon which the certification of death on neurological grounds is based is that of permanent cessation of all function in all parts of the brain—whole brain death—with which the reductionist United Kingdom concept should not be confused. The United States' President's Council on Bioethics made it clear, in its White Paper of December 2008, that the United Kingdom concept and clinical criteria are not considered sufficient for the diagnosis of death in the United States of America.

A focal impaired awareness seizure is a seizure that is associated with unilateral cerebral hemisphere involvement and causes impairment of awareness or responsiveness, i.e. alteration of consciousness.

- Presentation

Focal impaired awareness seizures are often preceded by an aura. The seizure aura is a focal aware seizure. The aura may manifest itself as a feeling of déjà vu, jamais vu, fear, euphoria or depersonalization. The aura might also occur as a visual disturbance, such as tunnel vision or a change in the perceived size of objects. Once consciousness is impaired, the person may display automatisms such as lip smacking, chewing or swallowing. There may also be loss of memory (amnesia) surrounding the seizural event. The person may still be able to perform routine tasks such as walking, although such movements are not purposeful or planned. Witnesses may not recognize that anything is wrong.

Focal impaired awareness seizures might arise from any lobe of the brain. They most commonly arise from the temporal lobe, particularly the amygdala, hippocampus, and neocortical regions. A common associated brain abnormality is mesial temporal sclerosis. Mesial temporal sclerosis is a specific pattern of hippocampal neuronal loss accompanied by hippocampal gliosis and atrophy. Focal onset impaired awareness seizures occur when excessive and synchronous electrical brain activity causes the impaired awareness and responsiveness. The abnormal electrical activity might spread to the rest of the brain and cause a "focal to bilateral seizure" or a generalized tonic–clonic seizure. The newer classification of 2017 groups only focal and generalized seizures, and generalised seizures are those that involve both sides of the brain from the onset.

A neurological disorder is any disorder of the nervous system. Structural, biochemical or electrical abnormalities in the brain, spinal cord or other nerves can result in a range of symptoms. Examples of symptoms include paralysis, muscle weakness, poor coordination, loss of sensation, seizures, confusion, pain and altered levels of consciousness. There are many recognized neurological disorders, some relatively common, but many rare. They may be assessed by neurological examination, and studied and treated within the specialities of neurology and clinical neuropsychology.

Interventions for neurological disorders include preventative measures, lifestyle changes, physiotherapy or other therapy, neurorehabilitation, pain management, medication, or operations performed by neurosurgeons. The World Health Organization estimated in 2006 that neurological disorders and their sequelae (direct consequences) affect as many as one billion people worldwide, and identified health inequalities and social stigma/discrimination as major factors contributing to the associated disability and suffering.

Patients who experience full awareness with explicit recall may have suffered an enormous trauma. Some patients experience post traumatic stress disorder (PTSD), leading to long-lasting after-effects such as nightmares, night terrors, flashbacks, insomnia, and in some cases even suicide. Some cases of awareness alert the patient to intra-operative errors.

A study from Sweden in 2002 attempted to follow up 18 patients for approximately 2 years after having been previously diagnosed with awareness under anesthesia. Four of the nine interviewed patients were still severely disabled due to psychiatric/psychological after-effects. All of these patients had experienced anxiety during the period of awareness, but only one had stated feeling pain. Another three patients had less severe, transient mental symptoms, although they could cope with these in daily life. Two patients denied any lasting effects from their awareness episode.

Absence seizures are one of several kinds of seizures. These seizures are sometimes referred to as petit mal seizures (from the French for "little illness", a term dating from the late 18th century). Absence seizures are characterized by a brief loss and return of consciousness, generally not followed by a period of lethargy (i.e. without a notable postictal state).