Published epidemiological data for akathisia are mostly limited to treatment periods preceding the arrival of second-generation antipsychotics. Sachdev (1995) reported an incidence rate of acute akathisia of 31% for 100 patients treated for 2 weeks with antipsychotic medications. Sachdev (1995) reported a prevalence range from 0.1% to 41%. In all likelihood, rates of prevalence are lower for current treatment as second-generation antipsychotics carry a lower risk of akathisia.

Psychomotor retardation (also known as "psychomotor impairment" or "motormental retardation") involves a slowing-down of thought and a reduction of physical movements in an individual. Psychomotor retardation can cause a visible slowing of physical and emotional reactions, including speech and affect. This is most-commonly seen in people with major depression and in the depressed phase of bipolar disorder; it is also associated with the adverse effects of certain drugs, such as benzodiazepines. Particularly in an inpatient setting, psychomotor retardation may require increased nursing care to ensure adequate food and fluid intake and sufficient personal care. Informed consent for treatment is more difficult to achieve in the presence of this condition.

Akathisia is frequently associated with the use of dopamine receptor antagonist antipsychotic drugs. Understanding is still limited on the pathophysiology of akathisia, but it is seen to be associated with medications which block dopaminergic transmission in the brain. Additionally, drugs with successful therapeutic effects in the treatment of medication-induced akathisia have provided additional insight into the involvement of other transmitter systems. These include benzodiazepines, β-adrenergic blockers, and serotonin antagonists. Another major cause of the syndrome is the withdrawal observed in drug dependent individuals. Since dopamine deficiency (or disruptions in dopamine signalling) appears to play an important role in the development of RLS, a form of akathisia focused in the legs, the sudden withdrawal or rapidly decreased dosage of drugs which increase dopamine signalling may create similar deficits of the chemical which mimic dopamine antagonism and thus can precipitate RLS. This is why sudden cessation of opioids, cocaine, serotonergics, and other euphoria-inducing substances commonly produce RLS as a side-effect.

It has been correlated with Parkinson's disease and related syndromes. It is unclear, however, whether this is due more to Parkinson's or the drugs used to treat it, such as carbidopa/levodopa (levocarb).

Antidepressants can also induce the appearance of akathisia, due to increased serotonin signalling within the central nervous system. This also explains why serotonin antagonists are often a very effective treatment.

The 2006 UK study by Healy et al. observed that akathisia is often miscoded in antidepressant clinical trials as "agitation, emotional lability, and hyperkinesis (overactivity)". The study further points out that misdiagnosis of akathisia as simple motor restlessness occurs, but that this is more properly classed as dyskinesia.

It was discovered that akathisia involves increased levels of the neurotransmitter norepinephrine, which is associated with mechanisms that regulate aggression, alertness, and arousal.

The table below summarizes factors that can induce akathisia, grouped by type, with examples or brief explanations for each:

Causes include:

- Schizophrenia

- Bipolar disorder

- Excited delirium

- Post-traumatic stress disorder (PTSD)

- Panic attacks

- Anxiety disorder

- Obsessive-compulsive disorder (OCD)

- Alcohol withdrawal

- Claustrophobia

- Dementia

- Parkinson's disease

- Traumatic brain injury

- Alzheimer's disease

- Acute intermittent porphyria

- Hereditary coproporphyria

- Variegate porphyria

- Side effects of drugs like cocaine or methylphenidate

- Side effects of antipsychotics like haloperidol

Examples of psychomotor retardation include the following:

- Unaccountable difficulty in carrying out what are usually considered "automatic" or "mundane" self-care tasks for healthy people (i.e., without depressive illness) such as taking a shower, dressing, self-grooming, cooking, brushing one's teeth and exercising.

- Physical difficulty performing activities which normally would require little thought or effort such as walking up a flight of stairs, getting out of bed, preparing meals and clearing dishes from the table, household chores or returning phone calls.

- Tasks requiring mobility suddenly (or gradually) and inexplicably seem to be "impossible". Activities such as shopping, getting groceries, caring for the daily needs of one's children and meeting the demands of employment or school are commonly affected. Individuals experiencing these symptoms typically sense that something is wrong, and may be confused about their inability to perform these tasks.

- Activities usually requiring little mental effort can become challenging. Balancing one's checkbook, making a shopping list or making decisions about mundane tasks (such as deciding what errands need to be done) are often difficult.

In schizophrenia, activity level may vary from psychomotor retardation to agitation; the patient will experience periods of listlessness and may be unresponsive, and at the next moment be active and energetic.

Intramuscular midazolam, lorazepam, or another benzodiazepine can be used to both sedate agitated patients, and control semi-involuntary muscle movements in cases of suspected akathisia.

Droperidol, haloperidol, or other typical antipsychotics can decrease the duration of agitation caused by acute psychosis, but should be avoided if the agitation is suspected to be akathisia, which can be potentially worsened. Also using promethazine may be useful.

In those with psychosis causing agitation there is a lack of support for the use of benzodiazepines, although they can prevent side effects associated with dopamine antagonists.

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

Epidemiological studies of serotonin syndrome are difficult as many physicians are unaware of the diagnosis or they may miss the syndrome due to its variable manifestations. In 1998 a survey conducted in England found that 85% of the general practitioners that had prescribed the antidepressant nefazodone were unaware of serotonin syndrome. The incidence may be increasing as a larger number of pro-serotonergic drugs (drugs which increase serotonin levels) are now being used in clinical practice. One postmarketing surveillance study identified an incidence of 0.4 cases per 1000 patient-months for patients who were taking nefazodone. Additionally, around 14 to 16 percent of persons who overdose on SSRIs are thought to develop serotonin syndrome.

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

Drugs that can trigger an oculogyric crisis include neuroleptics (such as haloperidol, chlorpromazine, fluphenazine, olanzapine), carbamazepine, chloroquine, cisplatin, diazoxide, levodopa, lithium, metoclopramide, lurasidone, domperidone, nifedipine, pemoline, phencyclidine ("PCP"), reserpine, and cetirizine, an antihistamine. High-potency neuroleptics are probably the most common cause in the clinical setting.

Other causes can include postencephalitic Parkinson's, Tourette's syndrome, multiple sclerosis, neurosyphilis, head trauma, bilateral thalamic infarction, lesions of the fourth ventricle, cystic glioma of the third ventricle, herpes encephalitis, kernicterus and juvenile Parkinson's.

Initial treatment is aimed at providing symptomatic relief. Benzodiazepines are the first line of treatment, and high doses are often required. A test dose of intramuscular lorazepam will often result in marked improvement within half an hour. In France, zolpidem has also been used in diagnosis, and response may occur within the same time period. Ultimately the underlying cause needs to be treated.

Electroconvulsive therapy (ECT) is an effective treatment for catatonia. Antipsychotics should be used with care as they can worsen catatonia and are the cause of neuroleptic malignant syndrome, a dangerous condition that can mimic catatonia and requires immediate discontinuation of the antipsychotic.

Excessive glutamate activity is believed to be involved in catatonia; when first-line treatment options fail, NMDA antagonists such as amantadine or memantine are used. Amantadine may have an increased incidence of tolerance with prolonged use and can cause psychosis, due to its additional effects on the dopamine system. Memantine has a more targeted pharmacological profile for the glutamate system, reduced incidence of psychosis and may therefore be preferred for individuals who cannot tolerate amantadine. Topiramate is another treatment option for resistant catatonia; it produces its therapeutic effects by producing glutamate antagonism via modulation of AMPA receptors.

Upon the discontinuation of serotonergic drugs, most cases of serotonin syndrome resolve within 24 hours, although in some cases delirium may persist for a number of days. Symptoms typically persist for a longer time frame in patients taking drugs which have a long elimination half-life, active metabolites, or a protracted duration of action.

Cases have reported muscle pain and weakness persisting for months, and antidepressant discontinuation may contribute to ongoing features. Following appropriate medical management, serotonin syndrome is generally associated with a favorable prognosis.

Catatonia is a state of psycho-motor immobility and behavioral abnormality manifested by stupor. It was first described in 1874 by Karl Ludwig Kahlbaum, in ("Catatonia or Tension Insanity").

Though catatonia has historically been related to schizophrenia (catatonic schizophrenia), it is now known that catatonic symptoms are nonspecific and may be observed in other mental disorders and neurological conditions. In the fifth edition of the "Diagnostic and Statistical Manual of Mental Disorders" (DSM), catatonia is not recognized as a separate disorder, but is associated with psychiatric conditions such as schizophrenia (catatonic type), bipolar disorder, post-traumatic stress disorder, depression and other mental disorders, narcolepsy, as well as drug abuse or overdose (or both). It may also be seen in many medical disorders including infections (such as encephalitis), autoimmune disorders, focal neurologic lesions (including strokes), metabolic disturbances, alcohol withdrawal and abrupt or overly rapid benzodiazepine withdrawal. In the fifth edition of the DSM, it is written that a variety of medical conditions may cause catatonia, especially neurological conditions: encephalitis, cerebrovascular disease, neoplasms, head injury. Moreover, metabolic conditions: homocystinuria, diabetic ketoacidosis, hepatic encephalopathy, hypercalcaemia.

It can be an adverse reaction to prescribed medication. It bears similarity to conditions such as encephalitis lethargica and neuroleptic malignant syndrome. There are a variety of treatments available; benzodiazepines are a first-line treatment strategy. Electroconvulsive therapy is also sometimes used. There is growing evidence for the effectiveness of NMDA receptor antagonists for benzodiazepine-resistant catatonia. Antipsychotics are sometimes employed but require caution as they can worsen symptoms and have serious adverse effects.

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.

Delirium arises through the interaction of a number of predisposing and precipitating factors. A predisposing factor might be any biological, psychological or social factor that increases an individual’s susceptibility to delirium. An individual with multiple predisposing factors is said to have "high baseline vulnerability". A precipitating factor is any biological, psychological or social factor that can trigger delirium. The division of causes into "predisposing" and "precipitating" is useful in order to assess an individual’s risk of suffering from delirium, and in guiding the management of delirium – however there may be a significant degree of overlap between the two categories.

Delirium most commonly affects the old age and those of ill health. Health results from physical and socioeconomic assets, and opposing factors come from physical and socioeconomic deficits. Individuals with significant predisposing factors don't compensate for physical or social stressors ("precipitating factors"). In such an individual, a single or mild precipitating factor could be sufficient to trigger an episode of delirium. Conversely, delirium may only result in a healthy individual if they suffer serious or multiple precipitating factors. It is important to note that the factors affecting those of an individual can change over time, thus an individual’s risk of delirium is in a state of flux.

Oculogyric crisis (OGC) is the name of a dystonic reaction to certain drugs or medical conditions characterized by a prolonged involuntary upward deviation of the eyes. The term "oculogyric" refers to the bilateral elevation of the visual gaze, but several other responses are associated with the crisis.

Epilepsy can manifest as oculogyric seizures, also called versive seizures.

The most important predisposing factors are listed below:

- Older age

- Cognitive impairment / dementia

- Physical comorbidity (biventricular failure, cancer, cerebrovascular disease)

- Psychiatric comorbidity (e.g., depression)

- Sensory impairment (vision, hearing)

- Functional dependence (e.g., requiring assistance for self-care and/or mobility)

- Dehydration / malnutrition

- Drugs and drug-dependence.

- Alcohol dependence

Antibodies against voltage-gated potassium channels (VGKC), which are detectable in about 40% of patients with acquired neuromytonia, have been implicated in Morvan’s pathophysiology. Raised serum levels of antibodies to VGKCs have been reported in three patients with Morvan’s Syndrome. Binding of serum from a patient with Morvan’s Syndrome to the hippocampus in a similar pattern of antibodies to known VGKC suggest that these antibodies can also cause CNS dysfunction. Additional antibodies against neuromuscular junction channels and receptors have also been described. Experimental evidence exists that these anti-VGKC antibodies cause nerve hyperexcitability by suppression of voltage gated K+ outward currents, whereas other, yet undefined humoral factors have been implicated in anti-VGKC antibody negative neuromyotonia. It is believed that antibodies to the Shaker-type K+ channels (the Kv1 family) are the type of potassium channel most strongly associated with acquired neuromyotonia and Morvan’s Syndrome.

Whether VGKC antibodies play a pathogenic role in the encephalopathy as they do in the peripheral nervous system is as yet unclear. It has been suggested that the VGKC antibodies may cross the blood–brain barrier and act centrally, binding predominantly to thalamic and striatal neurons causing encephalopathic and autonomic features.

Dravet syndrome is a severe form of epilepsy. It is a rare genetic disorder that affects an estimated 1 in every 20,000–40,000 births.

Excited delirium occurs most commonly in males with a history of serious mental illness or acute or chronic drug abuse, particularly stimulant drugs such as cocaine and MDPV. Alcohol withdrawal or head trauma may also contribute to the condition.

A majority of fatal case involved men.

People with excited delirium commonly have acute drug intoxication, generally involving PCP, methylenedioxypyrovalerone (MDPV), cocaine, or methamphetamine. Other drugs that may contribute to death are antipsychotics.

In one case, a patient was diagnosed with both Morvan's syndrome and pulmonary hyalinizing granulomas (PHG). PHG are rare fibrosing lesions of the lung, which have central whorled deposits of lamellar collagen. How these two diseases relate to one another is still unclear.

Thymoma, prostate adenoma, and in situ carcinoma of the sigmoid colon have also been found in patients with Morvan’s Syndrome.

The pathophysiology of excited delirium has been unclear, but likely involves multiple factors. These may include positional asphyxia, hyperthermia, drug toxicity, and/or catecholamine-induced fatal cardiac arrhythmias.

Dravet syndrome, also known as severe myoclonic epilepsy of infancy (SMEI), is a type of epilepsy with seizures that are often triggered by hot temperatures or fever. It is treated with anticonvulsant medications. It often begins around six months of age.

The cause of benign paroxysmal torticollis in infants is thought to be migrainous. More than 50% of infants have a family history of migraine in first degree relatives. The cause is likely to be genetic.

In affected individuals presenting with the ICCA syndrome, the human genome was screened with microsatellite markers regularly spaced, and strong evidence of linkage with the disease was obtained in the pericentromeric region of chromosome 16, with a maximum lod score, for D16S3133 of 6.76 at a recombination fraction of 0. The disease gene has been mapped at chromosome 16p12-q12.This linkage has been confirmed by different authors. The chromosome 16 ICCA locus shows complicated genomic architecture and the ICCA gene remains unknown.