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.

In the initial assessment of coma, it is common to gauge the level of consciousness by spontaneously exhibited actions, response to vocal stimuli ("Can you hear me?"), and painful stimuli; this is known as the AVPU (alert, vocal stimuli, painful stimuli, unresponsive) scale. More elaborate scales, such as the Glasgow Coma Scale, quantify an individual's reactions such as eye opening, movement and verbal response on a scale; Glasgow Coma Scale (GCS) is an indication of the extent of brain injury varying from 3 (indicating severe brain injury and death) to a maximum of 15 (indicating mild or no brain injury).

In those with deep unconsciousness, there is a risk of asphyxiation as the control over the muscles in the face and throat is diminished. As a result, those presenting to a hospital with coma are typically assessed for this risk ("airway management"). If the risk of asphyxiation is deemed high, doctors may use various devices (such as an oropharyngeal airway, nasopharyngeal airway or endotracheal tube) to safeguard the airway.

Examination reveals decreased muscle tone of the extremities and depression of tendon reflexes. Pupillary reaction to light may be sluggish, but the corneal reflexes are preserved. Depending on the nature and extent of brain damage, symptoms of pyramidal impairment may be present (e.g. paresis, Babinski sign).

If not stimulated externally, a patient with stupor will be in a sleepy state most of the time. In some extreme cases of severe depressive disorders the patient can become motionless, lose their appetite and become mute. Short periods of restricted responsivity can be achieved by intense stimulation (e.g. pain, bright light, loud noise, shock).

The patient does not respond to the environment, perform any tasks, or respond to questions.

The ability to swallow is maintained.

Lesions of the ascending reticular activation system on height of the pons and metencephalon have been shown to cause stupor. The incidence is higher after left-sided lesions.

People with catatonia may experience an extreme loss of motor skill or even constant hyperactive motor activity. Catatonic patients will sometimes hold rigid poses for hours and will ignore any external stimuli. People with catatonic excitement can suffer from exhaustion if not treated. Patients may also show stereotyped, repetitive movements.

They may show specific types of movement such as waxy flexibility, in which they maintain positions after being placed in them by someone else. Conversely, they may remain in a fixed position by resisting movement in proportion to the force applied by the examiner. They may repeat meaningless phrases or speak only to repeat what the examiner says.

While catatonia is only identified as a symptom of schizophrenia in present psychiatric classifications, it is increasingly recognized as a syndrome with many faces. It appears as the Kahlbaum syndrome (motionless catatonia), malignant catatonia (neuroleptic malignant syndrome, toxic serotonin syndrome), and excited forms (delirious mania, catatonic excitement, oneirophrenia).

It has also been recognized as grafted on to autism spectrum disorders.

Fink and Taylor developed a catatonia rating scale to identify the syndrome. A diagnosis is verified by a benzodiazepine or barbiturate test. The diagnosis is validated by the quick response to either benzodiazepines or electroconvulsive therapy (ECT). While proven useful in the past, barbiturates are no longer commonly used in psychiatry; thus the option of either benzodiazepines or ECT.

Complex partial status epilepticus (CPSE) is one of the non-convulsive forms of status epilepticus, a rare form of epilepsy defined by its recurrent nature. CPSE is characterized by seizures involving long-lasting stupor, staring and unresponsiveness. Sometimes this is accompanied by motor automatisms, such as eye twitching.

Convulsive status epilepticus presents with a regular pattern of contraction and extension of the arms and legs.

Epilepsia partialis continua is a variant involving hour-, day-, or even week-long jerking. It is a consequence of vascular disease, tumors, or encephalitis, and is drug-resistant.

Generalized myoclonus is commonly seen in comatose people following CPR and is seen by some as an indication of catastrophic damage to the neocortex.

Refractory status epilepticus is defined as status epilepticus that continues despite treatment with benzodiazepines and one antiepileptic drug.

Super-refractory status epilepticus is defined as status epilepticus that continues or recurs 24 hours or more after the onset of anaesthetic therapy, including those cases where status epilepticus recurs on the reduction or withdrawal of anesthesia.

Nonconvulsive status epilepticus is a relatively long duration change in a person's level of consciousness without large scale bending and extension of the limbs due to seizure activity. It is of two main types with either prolonged complex partial seizures or absence seizures. Up to a quarter of cases of SE are nonconvulsive.

In the case of complex partial status epilepticus, the seizure is confined to a small area of the brain, normally the temporal lobe. Absence status epilepticus is marked by a generalized seizure affecting the whole brain. An EEG is needed to differentiate between the two conditions. This results in episodes characterized by a long-lasting stupor, staring, and unresponsiveness.

List of symptoms that has been observed in those with autistic catatonia:

- Stupor

- Mutism

- Hyperactivity

- Agitation

- Excitement

- Posing

- Negativism

- Rigidity

- Waxy flexibility

- Automatic obedience

- Combativeness (during excitement)

- Aggressivity

- Stereotypies

- Tics

- Grimacing

- Echolalia

- Echopraxia

- Perseveration

- Verbigeration

- Staring

- Withdrawal

- Immobility

- Challenging behaviour

- Tremor

- Slowness

- Amotivation

- Grasp reflex

- Mannerism

- Gaze fixation

- Choreoathetoid movements of the trunk and extremities

- Autonomic instability (during excitement)

- Cannot start actions

- Cannot stop actions (if during excitement episodes needs acute psychiatric care)

- Freezing

- Impulsivity

- Bizarre/psychotic

- Sleep problems

- Urinary or Fecal incontinence

- Odd gait

- Passivity

- Reversal of day and night

- Eyerolling

- Stiff muscles

- Catalepsy

- Physiological pillow

- Difficulty crossing lines

- Gegenhalten

- Mitgehen

- Mitmachen

- Ambitendency

- Rituals

The symptoms of an opiate toxidrome include the classic triad of coma, pinpoint pupils, and respiratory depression as well as altered mental states, shock, pulmonary edema and unresponsiveness. Complications include bradycardia, hypotension, and hypothermia. Substances that may cause this toxidrome are opioids.

Waxy flexibility is a psychomotor symptom of catatonia as associated with schizophrenia, bipolar disorder, or other mental disorders which leads to a decreased response to stimuli and a tendency to remain in an immobile posture. Attempts to reposition the patient are met by "slight, even resistance", and after being repositioned the patient will typically remain in the new position. Waxy flexibility rarely occurs in cases of delirium. The presence of waxy flexibility along with at least two other catatonic symptoms such as stupor or negativism are enough to warrant a diagnosis of catatonia.

For instance, if one were to move the arm of someone with waxy flexibility, they would keep their arm where one moved it until it was moved again, as if it were made from wax. Further alteration of an individual's posture is similar to bending a candle. Although waxy flexibility has historically been linked to schizophrenia, there are also other disorders which it may be associated with, for example, mood disorder with catatonic behaviour.

Electroconvulsive therapy is often used as a treatment for catatonia. A study has found that catatonic patients suffering from waxy flexibility responded faster to electroconvulsive therapy, compared to patients with different catatonic symptoms.

The symptoms of a cholinergic toxidrome include bronchorrhea, confusion, defecation, diaphoresis, diarrhea, emesis, lacrimation, miosis, muscle fasciculations, salivation, seizures, urination, and weakness. Complications include bradycardia, hypothermia, and tachypnea. Substances that may cause this toxidrome include carbamates, mushrooms, and organophosphates.

Common mnemonics for organophosphate poisoning include the "killer B's" of bradycardia, bronchorrhea and bronchospasm because they are the leading cause of death, and SLUDGE - Salivation, Lacrimation, Urination, Diarrhea, Gastrointestinal distress, and Emesis.

An alternative mnemonic is DUMBBELLSS - Diarrhea, Urination, Miosis, Bradycardia, Bronchospasm, Emesis, Lacrimation, Lethargy, Salivation and Seizures.

As is the case with other non-convulsive status epilepticus forms, CPSE is dangerously underdiagnosed. This is due to the potentially fatal yet veiled nature of the symptoms. Usually, an electroencephalogram, or EEG, is needed to confirm a neurologist's suspicions. The EEG is also needed to differentiate between absence status epilepticus (which affects the entire brain), and CPSE, which only affects one region.

Low body temperature results in shivering becoming more violent. Muscle mis-coordination becomes apparent. Movements are slow and labored, accompanied by a stumbling pace and mild confusion, although the person may appear alert. Surface blood vessels contract further as the body focuses its remaining resources on keeping the vital organs warm. The subject becomes pale. Lips, ears, fingers, and toes may become blue.

Symptoms of mild hypothermia may be vague, with sympathetic nervous system excitation (shivering, high blood pressure, fast heart rate, fast respiratory rate, and contraction of blood vessels). These are all physiological responses to preserve heat. Increased urine production due to cold, mental confusion, and hepatic dysfunction may also be present. Hyperglycemia may be present, as glucose consumption by cells and insulin secretion both decrease, and tissue sensitivity to insulin may be blunted. Sympathetic activation also releases glucose from the liver. In many cases, however, especially in alcoholic patients, hypoglycemia appears to be a more common presentation. Hypoglycemia is also found in many hypothermic patients, because hypothermia may be a result of hypoglycemia.

Treatment consists of high-dose lorazepam or in some cases ECT. The response to the treatment is usually good, especially if detected early

This is described as a rare form of severe mental illness, with the following characteristics:

- Sudden onset in a previously asymptomatic person.

- Brief duration, with full recovery.

- Psychotic symptoms that can include confusion or hallucinations, mutism and stupor, delusions, or manic state. These are distinct from premenstrual tension, premenstrual syndrome, premenstrual (late luteal phase) depression or dysphoric disorder or menstrual mood disorder.

- Occurrence in rhythm with the menstrual cycle.

It shares clinical features with, and presents similarly to, postpartum psychosis. Researchers Deuchar and Brockington proposed that a sudden drop in levels of estrogen in the brain could be the trigger for both conditions.

The most common sleep disorders include:

- Bruxism, involuntarily grinding or clenching of the teeth while sleeping.

- Catathrenia, nocturnal groaning during prolonged exhalation.

- Delayed sleep phase disorder (DSPD), inability to awaken and fall asleep at socially acceptable times but no problem with sleep maintenance, a disorder of circadian rhythms. Other such disorders are advanced sleep phase disorder (ASPD), non-24-hour sleep–wake disorder (non-24) in the sighted or in the blind, and irregular sleep wake rhythm, all much less common than DSPD, as well as the situational shift work sleep disorder.

- Hypopnea syndrome, abnormally shallow breathing or slow respiratory rate while sleeping.

- Idiopathic hypersomnia, a primary, neurologic cause of long-sleeping, sharing many similarities with narcolepsy.

- Insomnia disorder (primary insomnia), chronic difficulty in falling asleep and/or maintaining sleep when no other cause is found for these symptoms. Insomnia can also be comorbid with or secondary to other disorders.

- Kleine–Levin syndrome, a rare disorder characterized by persistent episodic hypersomnia and cognitive or mood changes.

- Narcolepsy, including excessive daytime sleepiness (EDS), often culminating in falling asleep spontaneously but unwillingly at inappropriate times. About 70% of those who have narcolepsy also have cataplexy, a sudden weakness in the motor muscles that can result in collapse to the floor while retaining full conscious awareness.

- Night terror, "Pavor nocturnus", sleep terror disorder, an abrupt awakening from sleep with behavior consistent with terror.

- Nocturia, a frequent need to get up and urinate at night. It differs from enuresis, or bed-wetting, in which the person does not arouse from sleep, but the bladder nevertheless empties.

- Parasomnias, disruptive sleep-related events involving inappropriate actions during sleep, for example sleep walking, night-terrors and catathrenia.

- Periodic limb movement disorder (PLMD), sudden involuntary movement of arms and/or legs during sleep, for example kicking the legs. Also known as nocturnal myoclonus. See also Hypnic jerk, which is not a disorder.

- Rapid eye movement sleep behavior disorder (RBD), acting out violent or dramatic dreams while in REM sleep, sometimes injuring bed partner or self (REM sleep disorder or RSD).

- Restless legs syndrome (RLS), an irresistible urge to move legs. RLS sufferers often also have PLMD.

- Shift work sleep disorder (SWSD), a situational circadian rhythm sleep disorder. (Jet lag was previously included as a situational circadian rhythm sleep disorder, but it doesn't appear in DSM-5 (see Diagnostic and Statistical Manual of Mental Disorders)).

- Sleep apnea, obstructive sleep apnea, obstruction of the airway during sleep, causing lack of sufficient deep sleep, often accompanied by snoring. Other forms of sleep apnea are less common. When air is blocked from entering into the lungs, the individual unconsciously gasps for air and sleep is disturbed. Stops of breathing of at least ten seconds, 30 times within seven hours of sleep, classifies as apnea. Other forms of sleep apnea include central sleep apnea and sleep-related hypoventilation.

- Sleep paralysis, characterized by temporary paralysis of the body shortly before or after sleep. Sleep paralysis may be accompanied by visual, auditory or tactile hallucinations. Not a disorder unless severe. Often seen as part of narcolepsy.

- Sleepwalking or "somnambulism", engaging in activities normally associated with wakefulness (such as eating or dressing), which may include walking, without the conscious knowledge of the subject.

- Somniphobia, one cause of sleep deprivation, a dread/ fear of falling asleep or going to bed. Signs of the illness include anxiety and panic attacks before and during attempts to sleep.

Hypertensive encephalopathy is most commonly encountered in young and middle-aged people who have hypertension. Overall, the condition is rare even among people with hypertension. Studies report that from 0.5 to 15% of people with malignant hypertension develop hypertensive encephalopathy. With the development of methods for detection and treatment of hypertension, hypertensive encephalopathy has been becoming more rare.

Symptoms of hypertensive encephalopathy typically start to occur 12–48 hours after a sudden and sustained increase in blood pressure. The first manifestation of these symptoms is a severe headache. Headache occurs in greater than 75% of patients. The patient becomes restless. Alterations in consciousness may follow several hours later, which include impaired judgement and memory, confusion, somnolence and stupor. If the condition is not treated, these neurological symptoms may worsen and ultimately turn into a coma. Other symptoms may include increased irritability, vomiting, diplopia, seizures, twitching and myoclonus of the limbs. Alterations in vision (vision blurring, hemivisual field defects, color blindness, cortical blindness) are common. They occur in 4 out of 11 cases (Jellinek et al. 1964). Hemiparesis, intracerebral hemorrhage, aphasia may also occur, but they are less common.

Menstrual psychosis is a debated form of psychosis with a brief, sudden onset related to the menstrual cycle. The symptoms associated to it are dramatic and include delirium, mania or mutism. Most psychiatrists do not recognise the condition. Only 80 established cases are reported in medical literature and most of them were described by 19th Century physicians. It is thought to be linked with postpartum psychosis. This journal has been published looking at the 'evidence' for menstrual psychosis'.

Depending on the location of the brain lesion different symptoms are more frequent:

- Brainstem tegmentum. - Ocular: pupillary changes. Extraocular muscle palsy; gaze palsy: nystagmus.

- Hypothalamus. Medulla: dorsal nuc. of vagus. - Autonomic dysfunct.: temperature; cardiocirculatory; respiratory.

- Medulla: vestibular region. Cerebellum. - Ataxia.

- Dorsomedial nuc. of thalamus. Mammillary bodies. - Amnestic syndrome for recent memory.

Mamillary lesion are characteristic-small petechial hemorrhages are found.

- Diffuse cerebral dysfunction.- Altered cognition: global confusional state.

- Brainstem: periaqueductal gray.- Reduction of consciousness

- Hypothalamic lesions may also affect the immune system, which is known in alcohol abusers, causing dysplasias and infections.

A sleep disorder, or somnipathy, is a medical disorder of the sleep patterns of a person or animal. Some sleep disorders are serious enough to interfere with normal physical, mental, social and emotional functioning. Polysomnography and actigraphy are tests commonly ordered for some sleep disorders.

Disruptions in sleep can be caused by a variety of issues, from teeth grinding (bruxism) to night terrors. When a person suffers from difficulty falling asleep and/or staying asleep with no obvious cause, it is referred to as insomnia.

Sleep disorders are broadly classified into dyssomnias, parasomnias, circadian rhythm sleep disorders involving the timing of sleep, and other disorders including ones caused by medical or psychological conditions and sleeping sickness.

Some common sleep disorders include sleep apnea (stops in breathing during sleep), narcolepsy and hypersomnia (excessive sleepiness at inappropriate times), cataplexy (sudden and transient loss of muscle tone while awake), and sleeping sickness (disruption of sleep cycle due to infection). Other disorders include sleepwalking, night terrors and bed wetting. Management of sleep disturbances that are secondary to mental, medical, or substance abuse disorders should focus on the underlying conditions.