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).

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).

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.

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.

Disorders of consciousness are medical conditions that inhibit consciousness. Some define disorders of consciousness as any change from complete self-awareness to inhibited or absent self-awareness and arousal. This category generally includes minimally conscious state and persistent vegetative state, but sometimes also includes the less severe locked-in syndrome and more severe but rare chronic coma. Differential diagnosis of these disorders is an active area of biomedical research. Finally, brain death results in an irreversible disruption of consciousness. While other conditions may cause a moderate deterioration (e.g., dementia and delirium) or transient interruption (e.g., grand mal and petit mal seizures) of consciousness, they are not included in this category.

One of the defining characteristics of minimally conscious state is the more continuous improvement and significantly more favorable outcomes post injury when compared with vegetative state. One study looked at 100 patients with severe brain injury. At the beginning of the study, all the patients were unable to follow commands consistently or communicate reliably. These patients were diagnosed with either MCS or vegetative state based on performance on the JFK Coma Recovery Scale and the diagnostic criteria for MCS as recommended by the Aspen Consensus Conference Work-group. Both patient groups were further separated into those that suffered from traumatic brain injury and those that suffered from non-traumatic brain injures (anoxia, tumor, hydrocephalus, infection). The patients were assessed multiple times over a period of 12 months post injury using the Disability Rating Scale (DRS) which ranges from a score of 30=dead to 0=no disabilities. The results show that the DRS scores for the MCS subgroups showed the most improvement and predicted the most favorable outcomes 12 months post injury. Amongst those diagnosed with MCS, DRS scores were significantly lower for those with non-traumatic brain injuries in comparison to the vegetative state patients with traumatic brain injury. DRS scores were also significantly lower for the MCS non-traumatic brain injury group compared to the MCS traumatic brain injury group. Pairwise comparisons showed that DRS scores were significantly higher for those that suffered from non-tramuatic brain injuries than those with traumatic brain injuries. For the patients in vegetative states there were no significant differences between patients with non-traumatic brain injury and those with traumatic brain injuries. Out of the 100 patients studied, 3 patients fully recovered (had a DRS score of 0). These 3 patients were diagnosed with MCS and had suffered from traumatic brain injuries.

In summary, those with minimally conscious state and non-traumatic brain injuries will not progress as well as those with traumatic brain injuries while those in vegetative states have an all around lower to minimal chance of recovery.

Because of the major differences in prognosis described in this study, this makes it crucial that MCS be diagnosed correctly. Incorrectly diagnosing MCS as vegetative state may lead to serious repercussions related to clinical management.

Brain death is the complete loss of brain function (including involuntary activity necessary to sustain life). It differs from persistent vegetative state, in which the person is alive and some autonomic functions remain.

Brain death is used as an indicator of legal death in many jurisdictions, but it is defined inconsistently. Various parts of the brain may keep functioning when others do not anymore, and the term "brain death" has been used to refer to various combinations. For example, although a major medical dictionary says that "brain death" is synonymous with "cerebral death" (death of the cerebrum), the US National Library of Medicine Medical Subject Headings (MeSH) system defines brain death as including the brainstem. The distinctions can be important because, for example, in someone with a dead cerebrum but a living brainstem, the heartbeat and ventilation can continue unaided, whereas in whole-brain death (which includes brain stem death), only life support equipment would keep those functions going. Patients classified as brain-dead can have their organs surgically removed for organ donation.

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.

Comas can last from several days to several weeks. In more severe cases a coma may last for over five weeks, while some have lasted as long as several years. After this time, some patients gradually come out of the coma, some progress to a vegetative state, and others die. Some patients who have entered a vegetative state go on to regain a degree of awareness. Others remain in a vegetative state for years or even decades (the longest recorded period being 42 years).

The outcome for coma and vegetative state depends on the cause, location, severity and extent of neurological damage. A deeper coma alone does not necessarily mean a slimmer chance of recovery, because some people in deep coma recover well while others in a so-called milder coma sometimes fail to improve.

People may emerge from a coma with a combination of physical, intellectual, and psychological difficulties that need special attention. Recovery usually occurs gradually—patients acquire more and more ability to respond. Some patients never progress beyond very basic responses, but many recover full awareness. Regaining consciousness is not instant: in the first days, patients are only awake for a few minutes, and duration of time awake gradually increases. This is unlike the situation in many movies where people who awake from comas are instantly able to continue their normal lives. In reality, the coma patient awakes sometimes in a profound state of confusion, not knowing how they got there and sometimes suffering from dysarthria, the inability to articulate any speech, and with many other disabilities.

Predicted chances of recovery are variable owing to different techniques used to measure the extent of neurological damage. All the predictions are based on statistical rates with some level of chance for recovery present: a person with a low chance of recovery may still awaken. Time is the best general predictor of a chance of recovery: after four months of coma caused by brain damage, the chance of partial recovery is less than 15%, and the chance of full recovery is very low.

The most common cause of death for a person in a vegetative state is secondary infection such as pneumonia, which can occur in patients who lie still for extended periods.

There are reports of patients coming out of coma after long periods of time. After 19 years in a minimally conscious state, Terry Wallis spontaneously began speaking and regained awareness of his surroundings.

A brain-damaged man, trapped in a coma-like state for six years, was brought back to consciousness in 2003 by doctors who planted electrodes deep inside his brain. The method, called deep brain stimulation (DBS) successfully roused communication, complex movement and eating ability in the 38-year-old American man who suffered a traumatic brain injury. His injuries left him in a minimally conscious state (MCS), a condition akin to a coma but characterized by occasional, but brief, evidence of environmental and self-awareness that coma patients lack.

Comas lasting seconds to minutes result in post-traumatic amnesia (PTA) that lasts hours to days; recovery plateau occurs over days to weeks.

Comas that last hours to days result in PTA lasting days to weeks; recovery plateau occurs over months.

Comas lasting weeks result in PTA that lasts months; recovery plateau occurs over months to years.

Traumatic brain injury (TBI, physical trauma to the brain) can cause a variety of complications, health effects that are not TBI themselves but that result from it. The risk of complications increases with the severity of the trauma; however even mild traumatic brain injury can result in disabilities that interfere with social interactions, employment, and everyday living. TBI can cause a variety of problems including physical, cognitive, emotional, and behavioral complications.

Symptoms that may occur after a concussion – a minor form of traumatic brain injury – are referred to as post-concussion syndrome.

Generally, a person who is unable to voluntarily open the eyes, does not have a sleep-wake cycle, is unresponsive in spite of strong tactile (painful) or verbal stimuli, and who generally scores between 3 and 8 on the Glasgow Coma Scale is considered in a coma. Coma may have developed in humans as a response to injury to allow the body to pause bodily actions and heal the most immediate injuries before waking. It therefore could be a compensatory state in which the body's expenditure of energy is not superfluous. The severity and mode of onset of coma depends on the underlying cause. For instance, severe hypoglycemia (low blood sugar) or hypercapnia (increased carbon dioxide levels in the blood) initially cause mild agitation and confusion, but progress to obtundation, stupor, and finally, complete unconsciousness. In contrast, coma resulting from a severe traumatic brain injury or subarachnoid hemorrhage can be instantaneous. The mode of onset may therefore be indicative of the underlying cause.

It is very important for family members and health care professionals to be aware of natural movements also known as Lazarus sign or Lazarus reflex that can occur on a brain-dead person whose organs have been kept functioning by life support. The living cells that can cause these movements are not living cells from the brain or brain stem, these cells come from the spinal cord. Sometimes these body movements can cause false hope for the family members.

A brain-dead individual has no clinical evidence of brain function upon physical examination. This includes no response to pain and no cranial nerve reflexes. Reflexes include pupillary response (fixed pupils), oculocephalic reflex, corneal reflex, no response to the caloric reflex test, and no spontaneous respirations.

It is important to distinguish between brain death and states that may be difficult to differentiate from brain death, (such as barbiturate overdose, alcohol intoxication, sedative overdose, hypothermia, hypoglycemia, coma, and chronic vegetative states). Some comatose patients can recover to pre-coma or near pre-coma level of functioning, and some patients with severe irreversible neurological dysfunction will nonetheless retain some lower brain functions, such as spontaneous respiration, despite the losses of both cortex and brain stem functionality. Such is the case with anencephaly.

Note that brain electrical activity can stop completely, or drop to such a low level as to be undetectable with most equipment. An EEG will therefore be flat, though this is sometimes also observed during deep anesthesia or cardiac arrest. Although in the United States a flat EEG test is not required to certify death, it is considered to have confirmatory value. In the UK it is not considered to be of value because any continuing activity it might reveal in parts of the brain above the brain stem is held to be irrelevant to the diagnosis of death on the Code of Practice criteria.

The diagnosis of brain death needs to be rigorous, in order to be certain that the condition is irreversible. Legal criteria vary, but in general they require neurological examinations by two independent physicians. The exams must show complete and irreversible absence of brain function (brain stem function in UK), and may include two isoelectric (flat-line) EEGs 24 hours apart (less in other countries where it is accepted that if the cause of the dysfunction is a clear physical trauma there is no need to wait that long to establish irreversibility). The patient should have a normal temperature and be free of drugs that can suppress brain activity if the diagnosis is to be made on EEG criteria.

Also, a radionuclide cerebral blood flow scan that shows complete absence of intracranial blood flow must be considered with other exams – temporary swelling of the brain, particularly within the first 72 hours, can lead to a false positive test on a patient that may recover with more time.

CT angiography is neither required nor sufficient test to make the diagnosis.

A brainstem stroke syndrome is a condition involving a stroke of the brainstem. Because of their location, they often involve impairment both of the cranial nuclei and of the long tracts.

A person may have vertigo, dizziness and severe imbalance without the hallmark of most strokes – weakness on one side of the body. The symptoms of vertigo, dizziness or imbalance usually occur together; dizziness alone is not a sign of stroke. Brainstem stroke can also cause diplopia, slurred speech and decreased level of consciousness. A more serious outcome is locked-in syndrome.

Severe head injuries can lead to permanent vegetative states or death, therefore being able to recognize symptoms and get medical attention is very important. Symptoms of a severe closed-head injury include:

- coma

- seizures

- loss of consciousness

Because the brain swelling that produces these symptoms is often a slow process, these symptoms may not surface for days to weeks after the injury.

Common symptoms of a closed-head injury include:

- headache

- dizziness

- nausea

- slurred speech

- vomiting

Diffuse axonal injury (DAI) is a brain injury in which damage in the form of extensive lesions in white matter tracts occurs over a widespread area. DAI is one of the most common and devastating types of traumatic brain injury, and is a major cause of unconsciousness and persistent vegetative state after severe head trauma. It occurs in about half of all cases of severe head trauma and may be the primary damage that occurs in concussion. The outcome is frequently coma, with over 90% of patients with severe DAI never regaining consciousness. Those who do wake up often remain significantly impaired.

DAI can occur in every degree of severity from very mild or moderate to very severe. Concussion may be a milder type of diffuse axonal injury.

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.

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.

DAI is the result of traumatic shearing forces that occur when the head is rapidly accelerated or decelerated, as may occur in car accidents, falls, and assaults. Vehicle accidents are the most frequent cause of DAI; it can also occur as the result of child abuse such as in shaken baby syndrome.

Immediate disconnection of axons could be observed in severe brain injury, but the major damage of DAI is delayed secondary axon disconnections slowly developed over an extended time course. Tracts of axons, which appear white due to myelination, are referred to as white matter. Lesions in both grey and white matters are found in postmortem brains in CT and MRI exams.

Besides mechanical breaking of the axonal cytoskeleton, DAI pathology also includes secondary physiological changes such as interrupted axonal transport, progressive swellings and degeneration. Recent studies have linked these changes to twisting and misalignment of broken axon microtubules, as well as tau and APP deposition.

Diffuse axonal injury, or DAI, usually occurs as the result of an acceleration or deceleration motion, not necessarily an impact. Axons are stretched and damaged when parts of the brain of differing density slide over one another. Prognoses vary widely depending on the extent of damage.

Presentation varies according to the injury. Some patients with head trauma stabilize and other patients deteriorate. A patient may present with or without neurological deficit. Patients with concussion may have a history of seconds to minutes unconsciousness, then normal arousal. Disturbance of vision and equilibrium may also occur. Common symptoms of head injury include coma, confusion, drowsiness, personality change, seizures, nausea and vomiting, headache and a lucid interval, during which a patient appears conscious only to deteriorate later.

Symptoms of skull fracture can include:

- leaking cerebrospinal fluid (a clear fluid drainage from nose, mouth or ear) may be and is strongly indicative of basilar skull fracture and the tearing of sheaths surrounding the brain, which can lead to secondary brain infection.

- visible deformity or depression in the head or face; for example a sunken eye can indicate a maxillar fracture

- an eye that cannot move or is deviated to one side can indicate that a broken facial bone is pinching a nerve that innervates eye muscles

- wounds or bruises on the scalp or face.

- Basilar skull fractures, those that occur at the base of the skull, are associated with Battle's sign, a subcutaneous bleed over the mastoid, hemotympanum, and cerebrospinal fluid rhinorrhea and otorrhea.

Because brain injuries can be life-threatening, even people with apparently slight injuries, with no noticeable signs or complaints, require close observation; They have a chance for severe symptoms later on. The caretakers of those patients with mild trauma who are released from the hospital are frequently advised to rouse the patient several times during the next 12 to 24 hours to assess for worsening symptoms.

The Glasgow Coma Scale (GCS) is a tool for measuring degree of unconsciousness and is thus a useful tool for determining severity of injury. The Pediatric Glasgow Coma Scale is used in young children. The widely used PECARN Pediatric Head Injury/Trauma Algorithm helps physicians weigh risk-benefit of imaging in a clinical setting given multiple factors about the patient—including mechanism/location of injury, age of patient, and GCS score.

Illusory palinopsia is often worse with high stimulus intensity and contrast ratio in a dark adapted state. Multiple types of illusory palinopsia often co-exist in a patient and occur with other diffuse, persistent illusory symptoms such as halos around objects, dysmetropsia (micropsia, macropsia, pelopsia, or teleopsia), Alice in Wonderland Syndrome, visual snow, and oscillopsia. Illusory palinopsia consists of the following four symptom categories.

Cerebral hypoxia is a form of hypoxia (reduced supply of oxygen), specifically involving the brain; when the brain is completely deprived of oxygen, it is called "cerebral anoxia". There are four categories of cerebral hypoxia; they are, in order of severity: diffuse cerebral hypoxia (DCH), focal cerebral ischemia, cerebral infarction, and global cerebral ischemia. Prolonged hypoxia induces neuronal cell death via apoptosis, resulting in a hypoxic brain injury.

Cases of total oxygen deprivation are termed "anoxia", which can be hypoxic in origin (reduced oxygen availability) or ischemic in origin (oxygen deprivation due to a disruption in blood flow). Brain injury as a result of oxygen deprivation either due to hypoxic or anoxic mechanisms are generally termed hypoxic/anoxic injuries (HAI). Hypoxic ischemic encephalopathy (HIE) is a condition that occurs when the entire brain is deprived of an adequate oxygen supply, but the deprivation is not total. While HIE is associated in most cases with oxygen deprivation in the neonate due to birth asphyxia, it can occur in all age groups, and is often a complication of cardiac arrest.

Cerebral hypoxia can be caused by any event that severely interferes with the brain's ability to receive or process oxygen. This event may be internal or external to the body. Mild and moderate forms of cerebral hypoxia may be caused by various diseases that interfere with breathing and blood oxygenation. Severe asthma and various sorts of anemia can cause some degree of diffuse cerebral hypoxia. Other causes include status epilepticus, work in nitrogen-rich environments, ascent from a deep-water dive, flying at high altitudes in an unpressurized cabin without supplemental oxygen, and intense exercise at high altitudes prior to acclimatization.

Severe cerebral hypoxia and anoxia is usually caused by traumatic events such as choking, drowning, strangulation, smoke inhalation, drug overdoses, crushing of the trachea, status asthmaticus, and shock. It is also recreationally self-induced in the fainting game and in erotic asphyxiation.

- Transient ischemic attack (TIA), is often referred to as a "mini-stroke". The American Heart Association and American Stroke Association (AHA/ASA) refined the definition of transient ischemic attack. TIA is now defined as a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction. The symptoms of a TIA can resolve within a few minutes, unlike a stroke. TIAs share the same underlying etiology as strokes; a disruption of cerebral blood flow. TIAs and strokes present with the same symptoms such as contralateral paralysis (opposite side of body from affected brain hemisphere), or sudden weakness or numbness. A TIA may cause sudden dimming or loss of vision, aphasia, slurred speech, and mental confusion. The symptoms of a TIA typically resolve within 24 hours, unlike a stroke. Brain injury may still occur in a TIA lasting only a few minutes. Having a TIA is a risk factor for eventually having a stroke.

- Silent stroke is a stroke which does not have any outward symptoms, and the patient is typically unaware they have suffered a stroke. Despite its lack of identifiable symptoms, a silent stroke still causes brain damage and places the patient at increased risk for a major stroke in the future. In a broad study in 1998, more than 11 million people were estimated to have experienced a stroke in the United States. Approximately 770,000 of these strokes were symptomatic and 11 million were first-ever silent MRI infarcts or hemorrhages. Silent strokes typically cause lesions which are detected via the use of neuroimaging such as fMRI. The risk of silent stroke increases with age but may also affect younger adults. Women appear to be at increased risk for silent stroke, with hypertension and current cigarette smoking being predisposing factors.

Oneiroid syndrome, from the Ancient Greek "" ("oneiros", meaning "dream") and "" ("eidos", meaning "form, likeness"), is dream-like fantastic derangement of consciousness with illusions and hallucinations, catatonic symptoms and kaleidoscopic quality of psychopathological experiences. It's an element of the catatonic form of schizophrenia and presents with a dream-like or nightmare-like state as a background of intensive psychopathological experiences.

Oneiroid states were first described by the German physician Wilhelm Mayer-Gross in 1924. Mayer-Gross's 1924 habilitation on "Self-descriptions of Confusional States: the Oneiroid Form of Experience" () is considered the first monograph about oneiroid state. In this monograph the psychopathological method was used (German psychiatrists called that the "phenomenological method" – phänomenologische Methode).

The oneiroid syndrome, known to European and Russian psychiatrists, but all but forgotten in the USA.

Later in 1961 the Bulgarian psychiatrist S.T. Stoyanov studied the dynamics and the course of the oneiroid syndrome in "periodic", or recurrent schizophrenia (ICD-10).

According to this research the syndrome has six stages in its course:

1. initial general-somatic and vegetative disorder

2. delusional mood

3. affective-delusional depersonalisation and derealisation

4. fantastic-delusional and affective depersonalisation and derealisation

5. illusional depersonalisation and derealisation, and

6. catatonic-oneiroid state in the culmination.

In most of the cases of the oneiroid syndrome there were crude pathological changes in the electroencephalography (EEG).

The prognosis of oneiroid catatonia is optimal, in comparison with lucid catatonia.