Akathisia may range in intensity from a sense of disquiet or anxiety, to excruciating discomfort, particularly in the knees. Patients typically pace for hours because the pressure on the knees reduces the discomfort somewhat; once their knees and legs become fatigued and they are unable to continue pacing, they sit or lie down, although this does not relieve the akathisia. When misdiagnosis occurs in antipsychotic neuroleptic-induced akathisia, more antipsychotic may be prescribed, potentially worsening the symptoms. Neuro-psychologist Dennis Staker had drug-induced akathisia for two days. His description of his experience was this: "It was the worst feeling I have ever had in my entire life. I wouldn't wish it on my worst enemy." Many patients describe symptoms of neuropathic pain akin to fibromyalgia and restless legs syndrome. In Han et al. (2013), the authors describe restless legs syndrome's relation to akathisia, "Some researchers regard RLS as a 'focal akathisia' [in the legs]." Although these side effects disappear quickly and remarkably when the medication is stopped, tardive, or late-persisting akathisia may go on long after the offending drug is discontinued, sometimes for a period of years.

Healy, et al. (2006), described the following regarding akathisia: tension, insomnia, a sense of discomfort, motor restlessness, and marked anxiety and panic. Increased labile affect can result, such as weepiness.

Jack Henry Abbott (1981) describes the sensation:

In addition, not all observable restless motion is akathisia. For example, mania, agitated depression, and Attention Deficit Hyperactivity Disorder may look like akathisia, but the movements feel voluntary and not due to restlessness.

The presence and severity of akathisia can be measured using the Barnes Akathisia Scale, which assesses both objective and subjective criteria. Precise assessment of akathisia is problematic, as it is difficult to differentiate from a multitude of disorders with similar symptoms. In a study of movement disorders induced by neuroleptics, akathisia was found in only 26% of patients originally diagnosed with akathisia. The primary distinguishing features of akathisia in comparison with other syndromes are primarily subjective characteristics, such as the feeling of inner restlessness. Akathisia can commonly be mistaken for agitation secondary to psychotic symptoms or mood disorder, antipsychotic dysphoria, restless legs syndrome (RLS), anxiety, insomnia, drug withdrawal states, tardive dyskinesia, or other neurological and medical conditions.

Additionally, the controversial diagnosis of "pseudoakathisia" is given, as noted by Mark J. Garcia. In his article discussing akathisia among adults with severe and profound intellectual disability, he describes pseudoakathisia as "comprising all the symptoms of abnormal movements seen with akathisia, but without a sense of restlessness".

Tremor is most commonly classified by clinical features and cause or origin. Some of the better known forms of tremor, with their symptoms, include the following:

- Cerebellar tremor (also known as intention tremor) is a slow, broad tremor of the extremities that occurs at the end of a purposeful movement, such as trying to press a button or touching a finger to the tip of one’s nose. Cerebellar tremor is caused by lesions in or damage to the cerebellum resulting from stroke, tumor, or disease such as multiple sclerosis or some inherited degenerative disorder. It can also result from chronic alcoholism or overuse of some medicines. In classic cerebellar tremor, a lesion on one side of the brain produces a tremor in that same side of the body that worsens with directed movement. Cerebellar damage can also produce a “wing-beating” type of tremor called rubral or Holmes’ tremor — a combination of rest, action, and postural tremors. The tremor is often most prominent when the affected person is active or is maintaining a particular posture. Cerebellar tremor may be accompanied by other manifestations of ataxia, including dysarthria (speech problems), nystagmus (rapid, involuntary rolling of the eyes), gait problems and postural tremor of the trunk and neck. "Titubation" is tremor of the head and is of cerebellar origin.

- Dystonic tremor occurs in individuals of all ages who are affected by dystonia, a movement disorder in which sustained involuntary muscle contractions cause twisting and repetitive motions and/or painful and abnormal postures or positions. Dystonic tremor may affect any muscle in the body and is seen most often when the patient is in a certain position or moves a certain way. The pattern of dystonic tremor may differ from essential tremor. Dystonic tremors occur irregularly and often can be relieved by complete rest. Touching the affected body part or muscle may reduce tremor severity (a geste antagoniste). The tremor may be the initial sign of dystonia localized to a particular part of the body.

- Essential tremor (sometimes called benign essential tremor) is the most common of the more than 20 types of tremor. Although the tremor may be mild and nonprogressive in some people, in others, the tremor is slowly progressive, starting on one side of the body but affecting both sides within 3 years. The hands are most often affected but the head, voice, tongue, legs, and trunk may also be involved. Head tremor may be seen as a vertical or horizontal motion. Essential tremor may be accompanied by mild gait disturbance. Tremor frequency may decrease as the person ages, but the severity may increase, affecting the person’s ability to perform certain tasks or activities of daily living. Heightened emotion, stress, fever, physical exhaustion, or low blood sugar may trigger tremors or increase their severity. Onset is most common after age 40, although symptoms can appear at any age. It may occur in more than one family member. Children of a parent who has essential tremor have a 50 percent chance of inheriting the condition. Essential tremor is not associated with any known pathology.

- Orthostatic tremor is characterized by fast (>12 Hz) rhythmic muscle contractions that occur in the legs and trunk immediately after standing. Cramps are felt in the thighs and legs and the patient may shake uncontrollably when asked to stand in one spot. No other clinical signs or symptoms are present and the shaking ceases when the patient sits or is lifted off the ground. The high frequency of the tremor often makes the tremor look like rippling of leg muscles while standing. Orthostatic tremor may also occur in patients who have essential tremor, and there might be an overlap between these categories of tremor.

- Parkinsonian tremor is caused by damage to structures within the brain that control movement. This resting tremor, which can occur as an isolated symptom or be seen in other disorders, is often a precursor to Parkinson's disease (more than 25 percent of patients with Parkinson’s disease have an associated action tremor). The tremor, which is classically seen as a "pill-rolling" action of the hands that may also affect the chin, lips, legs, and trunk, can be markedly increased by stress or emotion. Onset is generally after age 60. Movement starts in one limb or on one side of the body and usually progresses to include the other side.

- Physiological tremor occurs in every normal individual and has no clinical significance. It is rarely visible and may be heightened by strong emotion (such as anxiety or fear), physical exhaustion, hypoglycemia, hyperthyroidism, heavy metal poisoning, stimulants, alcohol withdrawal or fever. It can be seen in all voluntary muscle groups and can be detected by extending the arms and placing a piece of paper on top of the hands. Enhanced physiological tremor is a strengthening of physiological tremor to more visible levels. It is generally not caused by a neurological disease but by reaction to certain drugs, alcohol withdrawal, or medical conditions including an overactive thyroid and hypoglycemia. It is usually reversible once the cause is corrected. This tremor classically has a frequency of about 10 Hz

- tremor (also called hysterical tremor) can occur at rest or during postural or kinetic movement. The characteristics of this kind of tremor may vary but generally include sudden onset and remission, increased incidence with stress, change in tremor direction and/or body part affected, and greatly decreased or disappearing tremor activity when the patient is distracted. Many patients with psychogenic tremor have a conversion disorder (see Posttraumatic stress disorder) or another psychiatric disease.

- Rubral tremor is characterized by coarse slow tremor which is present at rest, at posture and with intention. This tremor is associated with conditions which affect the red nucleus in the midbrain, classically unusual strokes.

Tremor can result from other conditions as well

- Alcoholism, excessive alcohol consumption, or alcohol withdrawal can kill certain nerve cells, resulting in a tremor known as asterixis. Conversely, small amounts of alcohol may help to decrease familial and essential tremor, but the mechanism behind it is unknown. Alcohol potentiates GABAergic transmission and might act at the level of the inferior olive.

- Tremor in peripheral neuropathy may occur when the nerves that supply the body’s muscles are traumatized by injury, disease, abnormality in the central nervous system, or as the result of systemic illnesses. Peripheral neuropathy can affect the whole body or certain areas, such as the hands, and may be progressive. Resulting sensory loss may be seen as a tremor or ataxia (inability to coordinate voluntary muscle movement) of the affected limbs and problems with gait and balance. Clinical characteristics may be similar to those seen in patients with essential tremor.

- Tobacco withdrawal symptoms include tremor.

- Most of the symptoms can also occur randomly when panicked.

The extrapyramidal system regulates posture and skeletal muscle tone. Extrapyramidal symptoms (also called extrapyramidal side effects) get their name because they are symptoms of disorders in this system.

Restless leg syndrome is a disorder in which patients feel uncomfortable or unpleasant sensations in the legs. These sensations usually occur in the evening, while the patient is sitting or lying down and relaxing. Patients feel like they have to move their legs to relieve the sensations, and walking generally makes the symptoms disappear. In many patients, this can lead to insomnia and excessive daytime sleepiness. This is a very common problem and can occur at any age.

Similarly, the syndrome akathisia ranges from mildly compulsive movement usually in the legs to intense frenzied motion. These movements are partly voluntary, and the individual typically has the ability to suppress them for short amounts of time. Like restless leg syndrome, relief results from movement.

Extrapyramidal symptoms (EPS), also known as extrapyramidal side effects (EPSE), are drug-induced movement disorders that include acute and tardive symptoms. These symptoms include dystonia (continuous spasms and muscle contractions), akathisia (motor restlessness), parkinsonism (characteristic symptoms such as rigidity), bradykinesia (slowness of movement), tremor, and tardive dyskinesia (irregular, jerky movements). Antipsychotics are often discontinued due to inefficacy and intolerable side effects such as extrapyramidal symptoms.

Since it is difficult to measure extrapyramidal symptoms, rating scales are commonly used to assess the severity of movement disorders. The Simpson-Angus Scale (SAS), Barnes Akathisia Rating Scale (BARS), Abnormal Involuntary Movement Scale (AIMS), and Extrapyramidal Symptom Rating Scale (ESRS) are rating scales frequently used for such assessment and are not weighted for diagnostic purposes; these scales can help physicians weigh the benefit/expected benefit of a medication against the degree of distress which the side effects are causing the patient, aiding in the decision to maintain, reduce, or discontinue the causative medication/s.

Tremor can be a symptom associated with disorders in those parts of the brain that control muscles throughout the body or in particular areas, such as the hands. Neurological disorders or conditions that can produce tremor include multiple sclerosis, stroke, traumatic brain injury, chronic kidney disease and a number of neurodegenerative diseases that damage or destroy parts of the brainstem or the cerebellum, Parkinson's disease being the one most often associated with tremor. Other causes include the use of drugs (such as amphetamines, cocaine, caffeine, corticosteroids, SSRIs) or alcohol, mercury poisoning, or the withdrawal of drugs such as alcohol or benzodiazepine. Tremors can also be seen in infants with phenylketonuria (PKU), overactive thyroid or liver failure. Tremors can be an indication of hypoglycemia, along with palpitations, sweating and anxiety.

Tremor can also be caused from lack of sleep, lack of vitamins, or increased stress. Deficiencies of magnesium and thiamine have also been known to cause tremor or shaking, which resolves when the deficiency is corrected. See magnesium in biology. Some forms of tremor are inherited and run in families, while others have no known cause. Tremors can also be caused by some spider bites, e.g. the redback spider of Australia.

Characteristics may include a rhythmic shaking in the hands, arms, head, legs, or trunk; shaky voice; and problems holding things such as a fork or pen. Some tremors may be triggered by or become exacerbated during times of stress or strong emotion, when the individual is physically exhausted, or during certain postures or movements.

Tremor may occur at any age but is most common in middle-age and older persons. It may be occasional, temporary, or occur intermittently. Tremor affects men and women equally.

Tardive dyskinesia is characterized by repetitive, involuntary movements. Some examples of these types of involuntary movements include:

- Grimacing

- Tongue movements

- Lip smacking

- Lip puckering

- Pursing of the lips

- Excessive eye blinking

Rapid, involuntary movements of the limbs, torso, and fingers may also occur. In some cases, an individual's legs can be so affected that walking becomes difficult or impossible. These symptoms are the opposite of patients who are diagnosed with Parkinson's disease. Parkinson's patients have difficulty moving, whereas tardive dyskinesia patients have difficulty not moving.

Respiratory irregularity, such as grunting and difficulty breathing, is another symptom associated with tardive dyskinesia, although studies have shown that the prevalence rate is relatively low.

Tardive dyskinesia is often misdiagnosed as a mental illness rather than a neurological disorder, and as a result patients are prescribed neuroleptic drugs, which increase the probability that the patient will develop a severe and disabling case, and shortening the typical survival period.

Other closely related neurological disorders have been recognized as variants of tardive dyskinesia. Tardive dystonia is similar to standard dystonia but permanent. Tardive akathisia involves painful feelings of inner tension and anxiety and a compulsive drive to move the body. In some extreme cases, afflicted individuals experience so much internal torture that they lose their ability to sit still. Tardive tourettism is a tic disorder featuring the same symptoms as Tourette syndrome. The two disorders are extremely close in nature and often can only be differentiated by the details of their respective onsets. Tardive myoclonus, a rare disorder, presents as brief jerks of muscles in the face, neck, trunk, and extremities.

"AIMS Examination": This test is used when psychotropic medications have been prescribed because patients sometimes develop tardive dyskinesia due to prolonged use of antipsychotic medications. The Abnormal Involuntary Movement Scale (AIMS) examination is a test used to identify the symptoms of tardive dyskinesia (TD). The test is not meant to tell whether there is an absence or presence of tardive dyskinesia. It just scales to level of symptoms indicated by the actions observed. The levels range from none to severe. The AIMS examination was constructed in the 1970s to measure involuntary facial, trunk, and limb movements. It is best to do this test before and after the administration of the psychotropic drugs. Taking the AIMS consistently can help to track severity of TD over time.

Wilson's disease (WD) is a rare inherited disorder in which patients have a problem metabolizing copper. In patients with WD, copper accumulates in the liver and other parts of the body, particularly the brain, eyes and kidneys. Upon accumulation in the brain, patients may experience speech problems, incoordination, swallowing problems, and prominent hyperkinetic symptoms including tremor, dystonia, and gait difficulties. Psychiatric disturbances such as irritability, impulsiveness, aggressiveness, and mood disturbances are also common.

Tardive dyskinesia (TD) is a disorder that results in involuntary, repetitive body movements. This may include grimacing, sticking out the tongue or smacking of the lips. Additionally there may be rapid jerking movements or slow writhing movements. In about 20% of people, decreased functioning results.

Tardive dyskinesia occurs in some people as a result of long-term use of neuroleptic medications (antipsychotics, metoclopramide). These medications are usually used for mental illness, but may also be given for gastrointestinal or neurological problems. The condition typically only develops after months to years of use. The diagnosis is based on the symptoms after ruling out other potential causes.

Efforts to prevent the condition include not using or using the lowest possible dose of neuroleptics. Treatment include stopping the neuroleptic medication if possible or switching to clozapine. Other medications such as valbenazine, tetrabenazine, or botulinum toxin may be used to lessen the symptoms. With treatment some see a resolution of symptoms while others do not.

Rates in those on atypical antipsychotics are about 20% while those on typical antipsychotics have rates of about 30%. Risk is greater in older people. The term "tardive dyskinesia" first came into use in 1964.

RLS sensations range from pain or an aching in the muscles, to "an itch you can't scratch", a "buzzing sensation", an unpleasant "tickle that won't stop", a "crawling" feeling, or limbs jerking while awake. The sensations typically begin or intensify during quiet wakefulness, such as when relaxing, reading, studying, or trying to sleep.

It is a "spectrum" disease with some people experiencing only a minor annoyance and others having major disruption of sleep and impairments in quality of life.

The sensations—and the need to move—may return immediately after ceasing movement or at a later time. RLS may start at any age, including childhood, and is a progressive disease for some, while the symptoms may remit in others. In a survey among members of the Restless Legs Syndrome Foundation, it was found that up to 45% of patients had their first symptoms before the age of 20 years.

- "An urge to move, usually due to uncomfortable sensations that occur primarily in the legs, but occasionally in the arms or elsewhere."

- "Motor restlessness, expressed as activity, which relieves the urge to move."

- "Worsening of symptoms by relaxation."

- "Variability over the course of the day-night cycle, with symptoms worse in the evening and early in the night."

- "Restless legs feel similar to the urge to yawn, situated in the legs or arms."

Individuals with RLS have higher rates of depression and anxiety disorders.

RLS is categorized as either primary or secondary.

- Primary RLS is considered idiopathic or with no known cause. Primary RLS usually begins slowly, before approximately 40–45 years of age and may disappear for months or even years. It is often progressive and gets worse with age. RLS in children is often misdiagnosed as growing pains.

- Secondary RLS often has a sudden onset after age 40, and may be daily from the beginning. It is most associated with specific medical conditions or the use of certain drugs (see below).

Symptom onset is usually rapid, often occurring within minutes of elevated serotonin levels. Serotonin syndrome encompasses a wide range of clinical findings. Mild symptoms may consist of increased heart rate, shivering, sweating, dilated pupils, myoclonus (intermittent jerking or twitching), as well as overresponsive reflexes. However, many of these symptoms may be side effects of the drug or drug interaction causing excessive levels of serotonin; not an effect of elevated serotonin itself. Tremor is a common side effect of MDMA's action on dopamine, whereas hyperreflexia is symptomatic of exposure to serotonin agonists. Moderate intoxication includes additional abnormalities such as hyperactive bowel sounds, high blood pressure and hyperthermia; a temperature as high as . The overactive reflexes and clonus in moderate cases may be greater in the lower limbs than in the upper limbs. Mental changes include hypervigilance or insomnia and agitation. Severe symptoms include severe increases in heart rate and blood pressure that may lead to shock. Temperature may rise to above in life-threatening cases. Other abnormalities include metabolic acidosis, rhabdomyolysis, seizures, renal failure, and disseminated intravascular coagulation; these effects usually arising as a consequence of hyperthermia.

The symptoms are often described as a clinical triad of abnormalities:

- Cognitive effects: headache, agitation, hypomania, mental confusion, hallucinations, coma

- Autonomic effects: shivering, sweating, hyperthermia, vasoconstriction, tachycardia, nausea, diarrhea.

- Somatic effects: myoclonus (muscle twitching), hyperreflexia (manifested by clonus), tremor.

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

Tardive dysphrenia, was proposed by the American neurologist Stanley Fahn, the head of the Division of Movements Disorders of the Neurological Institute of New York, in collaboration with the psychiatrist David V Forrest in the 1970s.

It originally was linked to a unique, rare, behavioral/mental neuroleptic drug-induced tardive syndrome observed in psychiatric patients (schizophrenia in particular) treated with the typical antipsychotic drugs or neuroleptics. Tardive dysphrenia is one of many neuroleptic-induced tardive syndromes, including tardive dyskinesia and the other already-recognized tardive dystonia, and tardive akathisia.

More recently, the Brazilian psychiatrist Leopoldo Hugo Frota, Adjunct Professor of Psychiatry at Federal University of Rio de Janeiro, extended the original Fahn's construct to enclose the — independently described but etiologically related concepts of — rebound psychosis, supersensitivity psychosis (Guy Chouinard) and schizophrenia pseudo-refractoriness (Heinz Lehmann & Thomas Ban) or secondary acquired refractoriness.

There is some disagreement in the psychiatric community regarding the diagnosis of tardive dysphrenia. Therefore, the following description should be considered general and tentative.

Tardive dysphrenia is characterized by a worsening of psychiatric symptoms that can be directly traced to the administration of antipsychotic medication.

Six symptoms are considered when diagnosing tardive dysphrenia:

A) The patient shows:

B) The symptoms are present for a full four weeks (full two weeks if successfully treated by immediate reinstitution or augmentation with a more potent drug and/or the rising of the previous drug) and contain any of these patterns:

C) Criteria A & B signs and symptoms emerge progressively with the administration of an oral antipsychotic drug or during the four-weeks period that follows its withdrawal (8 weeks for dépôt formulations).

D) There has been any exposure to a typical and/or atypical antipsychotic drug for at least three full months (full 12 weeks), or 1 full month (full 4 weeks) if the patient is sixty years old or older.

E) The clinical signs and symptoms cannot be attributed to another psychiatric condition, neurological condition, somatic illness, or severe stress. Also, exposure to other psychosis-inducing medicines must be excluded.

F) The signs and symptoms could not be better explained by an eventual previous psychiatric/neurological condition unfavorable natural evolution (i.e., Primary Refractory or poor prognosis Schizophrenia; severe Acute Mania; Dementia with Psychotic Symptoms) or by Neuroleptic Dysphoria.

People with discontinuation syndrome have been on an antidepressant for at least four weeks and have recently stopped taking the medication, whether abruptly, after a fast taper, or each time the medication is reduced on a slow taper. Commonly reported symptoms include flu-like symptoms (nausea, vomiting, diarrhea, headaches, sweating) and sleep disturbances (insomnia, nightmares, constant sleepiness). Sensory and movement disturbances have also been reported, including imbalance, tremors, vertigo, dizziness, and electric-shock-like experiences in the brain, often described by sufferers as "brain zaps". Mood disturbances such as dysphoria, anxiety, or agitation are also reported, as are cognitive disturbances such as confusion and hyperarousal.

In cases associated with sudden discontinuation of MAO inhibitors, acute psychosis has been observed. Over fifty symptoms have been reported.

Most cases of discontinuation syndrome last between one and four weeks, are relatively mild, and resolve on their own; in rare cases symptoms can be severe or extended. Paroxetine ("Paxil") and venlafaxine ("Effexor") seem to be particularly difficult to discontinue and prolonged withdrawal syndrome lasting over 18 months have been reported with paroxetine.

A 2009 Advisory Committee to the FDA found that online anecdotal reports of discontinuation syndrome related to duloxetine ("Cymbalta") included severe symptoms and exceeded prevalence of both paroxetine ("Paxil") and venlafaxine ("Effexor") reports by over 250% (although acknowledged this may have been influenced by duloxetine being a much newer drug). It also found that the safety information provided by the manufacturer not only neglected important information about managing discontinuation syndrome, but also explicitly advised against opening capsules, a practice required to gradually taper dosage.

Psychomotor agitation is a set of signs and symptoms that stem from mental tension and anxiety. The signs are unintentional and purposeless motions; the symptoms are emotional distress and restlessness. Typical manifestations include pacing around a room, wringing the hands, uncontrolled tongue movement, pulling off clothing and putting it back on, and other similar actions. In more severe cases, the motions may become harmful to the individual, such as ripping, tearing, or chewing at the skin around one's fingernails, lips, or other body parts to the point of bleeding. Psychomotor agitation is typically found in major depressive disorder or obsessive-compulsive disorder, and sometimes the manic phase in bipolar disorder, though it can also be a result of an excess intake of stimulants. It can also be caused by severe hyponatremia. The middle-aged and the elderly are more at risk to express it.

Serotonin syndrome (SS) is a group of symptoms that may occur following use of certain serotonergic medications or drugs. The degree of symptoms can range from mild to severe. Symptoms include high body temperature, agitation, increased reflexes, tremor, sweating, dilated pupils, and diarrhea. Body temperature can increase to greater than . Complications may include seizures and extensive muscle breakdown.

Serotonin syndrome is typically caused by the use of two or more serotonergic medications or drugs. This may include selective serotonin reuptake inhibitor (SSRI), serotonin norepinephrine reuptake inhibitor (SNRI), monoamine oxidase inhibitor (MAOI), tricyclic antidepressants (TCAs), amphetamines, pethidine (meperidine), tramadol, dextromethorphan, buspirone, L-tryptophan, 5-HTP, St. John's wort, triptans, ecstasy (MDMA), metoclopramide, ondansetron, or cocaine. It occurs in about 15% of SSRI overdoses. It is a predictable consequence of excess serotonin on the central nervous system (CNS). Onset of symptoms is typically within a day of the extra serotonin.

Diagnosis is based on a person's symptoms and history of medication use. Other conditions that can produce similar symptoms such as neuroleptic malignant syndrome, malignant hyperthermia, anticholinergic toxicity, heat stroke, and meningitis should be ruled out. No laboratory tests can confirm the diagnosis.

Initial treatment consists of discontinuing medications which may be contributing. In those who are agitated benzodiazepines may be used. If this is not sufficient, a serotonin antagonist such as cyproheptadine may be used. In those with a high body temperature active cooling measures may be needed. The number of cases of serotonin syndrome that occur each year is unclear. With appropriate treatment the risk of death is less than one percent. The high-profile case of Libby Zion, who is generally accepted to have died from serotonin syndrome, resulted in changes to graduate medical education in New York State.

Antidepressant discontinuation syndrome is a condition that can occur following the interruption, dose reduction, or discontinuation of antidepressant drugs, including selective serotonin re-uptake inhibitors (SSRIs) or serotonin–norepinephrine reuptake inhibitors (SNRIs). The symptoms can include flu-like symptoms and disturbances in sleep, senses, movement, mood, and thinking. In most cases symptoms are mild, short-lived, and resolve without treatment. More severe cases may be successfully treated by reintroduction of the drug, provided reintroduction is done in a timely fashion. Symptoms, including tardive akathisia, and Post SSRI Sexual Dysfunction (PSSD) may persist for months to years, yet may spontaneously resolve after prolonged presence.

The term dysphrenia was coined by the German medical specialist Karl Kahlbaum to designate a clinical picture in 19th-century psychiatry. Today the concept is still used in the western world as a lay generic synonym for mental disorder in adults, and as a term to describe different cognitive/verbal/behavioral deficits in children and adolescents. It is also used in the People's Republic of China, controversially, to identify a local medical diagnostic category. A number of followers of the Falun Gong cult and other social movements considered insurrectionary by the regime are said to have been diagnosed with dysphrenia.

The medical expression tardive dysphrenia was first proposed by the American neurologist Stanley Fahn and collaborators in the 1970s. It was originally linked to a unique and rare non-motor behavioral/mental neuroleptic drug-induced tardive syndrome observed in psychiatric patients—schizophrenia in particular—who had been treated with typical antipsychotics.

Tardive dysphrenia was conceived to precede tardive dyskinesia and the other already-known neuroleptic-induced tardive syndromes (tardive dystonia, tardive akathisia). More recently, the Brazilian psychiatrist Leopoldo Hugo Frota extended Fahn's original construct to encompass the independently described but etiologically related concepts of rebound psychosis, supersensitivity psychosis (Guy Chouinard), and schizophrenia pseudo-refractoriness (Heinz Lehmann & Thomas Ban) or secondary acquired refractoriness.

Childhood schizophrenia (also known as childhood-onset schizophrenia, and very early-onset schizophrenia) is a schizophrenia spectrum disorder that is characterized by loosening of associations, delusions, catatonic behavior and "negative symptoms", such as inappropriate or blunted affect, withdrawal and schizophrenic autism, anhedonia with onset before 13 years of age. The term "childhood-onset schizophrenia" and "very early-onset schizophrenia" are used to identify patients in whom the disorder manifests before the age of 13.

The disorder presents symptoms such as auditory and visual hallucinations, strange thoughts or feelings, and abnormal behavior, profoundly impacting the child's ability to function and sustain normal interpersonal relationships. Delusions are often not systematized and vague.. Among the actual psychotic symptoms seen in childhood schizophrenia auditory hallucinations are the most common. They are often presented in relatively simple form of akoasms (auditory hallucinations, such as noise, shots, knocks, etc.). It typically presents after the age of seven. About 50% of young children diagnosed with schizophrenia experience severe neuropsychiatric symptoms. Studies have demonstrated that diagnostic criteria are similar to those of adult schizophrenia. Diagnosis is based on behavior observed by caretakers and, in some cases depending on age, self reports.

Schizophrenia has no definite cause; however, certain risk factors such as family history seem to correlate. There is no known cure, but childhood schizophrenia is controllable with the help of behavioral therapies and medications.

Schizophrenia is a mental disorder that is expressed in abnormal mental functions and disturbed behavior.

The signs and symptoms of childhood schizophrenia are nearly the same as adult-onset schizophrenia. Some of the earliest signs that a young child may develop schizophrenia are lags in language and motor development. Some children engage in activities such as flapping the arms or rocking, and may appear anxious, confused, or disruptive on a regular basis. Children may experience symptoms such as hallucinations, but these are often difficult to differentiate from just normal imagination or child play. It is often difficult for children to describe their hallucinations or delusions, making very early-onset schizophrenia especially difficult to diagnose in the earliest stages. The cognitive abilities of children with schizophrenia may also often be lacking, with 20% of patients showing borderline or full intellectual disability.

Very early-onset schizophrenia refers to onset before the age of thirteen. The prodromal phase, which precedes psychotic symptoms, is characterized by deterioration in school performance, social withdrawal, disorganized or unusual behavior, a decreased ability to perform daily activities, a deterioration in self-care skills, bizarre hygiene and eating behaviors, changes in affect, a lack of impulse control, hostility and aggression, and lethargy.

Auditory hallucinations are the most common "positive symptom" in children. Positive symptoms have come to mean psychopathological disorders that are actively expressed, such as delusions, hallucinations, thought disorder etc.). A child's auditory hallucinations may include voices that are conversing with each other or voices that are speaking directly to the children themselves. Many children with auditory hallucinations believe that if they do not listen to the voices, the voices will harm them or someone else. Tactile and visual hallucinations seem relatively rare. The children often attribute the hallucinatory voices to a variety of beings, including family members or other people, evil forces ("the Devil", "a witch", "a spirit"), animals, characters from horror movies (Bloody Mary, Freddy Krueger) and less clearly recognizable sources ("bad things," "the whispers"). Command auditory hallucinations (also known as imperative hallucinations) were common and experienced by more than ½ of the group in a research at the Bellevue Hospital Center's Children's Psychiatric Inpatient Unit. And voices repeat and repeat: "Kill somebody!", "Kill her, kill her!". Delusions are reported in more than half of children with schizophrenia, but they are usually less complex than those of adults. Delusions often connected with hallucinatory experiences.. In a research delusions were characterized as persecutory for the most part, but some children reported delusions of control. Many said they were being tortured by the beings causing their visual and auditory hallucinations, some thought that if they disobeying their voices would cause them harm.

Some degree of thought disorder was observed in a test group of children in Bellevue Hospital. They displayed illogicality, tangentialiry (a serious disturbance in the associative thought process), and loosening of associations.

Negative ("deficit") symptoms in schizophrenia reflect mental deficit states such as apathy and aboulia, avolition, flattened affect, asthenia etc.

Schizoaffective disorder is defined by "mood disorder-free psychosis" in the context of a long-term psychotic and mood disorder. Psychosis must meet criterion A for schizophrenia which may include delusions, hallucinations, disorganized speech, thinking or behavior and negative symptoms. Both delusions and hallucinations are classic symptoms of psychosis. Delusions are false beliefs which are strongly held despite evidence to the contrary. Beliefs should not be considered delusional if they are in keeping with cultural beliefs. Delusional beliefs may or may not reflect mood symptoms (for example, someone experiencing depression may or may not experience delusions of guilt). Hallucinations are disturbances in perception involving any of the five senses, although auditory hallucinations (or "hearing voices") are the most common. A lack of responsiveness or negative symptoms include alogia (lack of spontaneous speech), blunted affect (reduced intensity of outward emotional expression), avolition (loss of motivation), and anhedonia (inability to experience pleasure). Negative symptoms can be more lasting and more debilitating than positive symptoms of psychosis.

Mood symptoms are of mania, hypomania, mixed episode, or depression, and tend to be episodic rather than continuous. A mixed episode represents a combination of symptoms of mania and depression at the same time. Symptoms of mania include elevated or irritable mood, grandiosity (inflated self-esteem), agitation, risk-taking behavior, decreased need for sleep, poor concentration, rapid speech, and racing thoughts. Symptoms of depression include low mood, apathy, changes in appetite or weight, disturbances in sleep, changes in motor activity, fatigue, guilt or feelings of worthlessness, and suicidal thinking.

Schizoaffective disorder (SZA, SZD or SAD) is a mental disorder characterized by abnormal thought processes and deregulated emotions. The diagnosis is made when the person has features of both schizophrenia and a mood disorder—either bipolar disorder or depression—but does not strictly meet diagnostic criteria for either alone. The bipolar type is distinguished by symptoms of mania, hypomania, or mixed episode; the depressive type by symptoms of depression only. Common symptoms of the disorder include hallucinations, paranoid delusions, and disorganized speech and thinking. The onset of symptoms usually begins in young adulthood, currently with an uncertain lifetime prevalence because the disorder was redefined, but DSM-IV prevalence estimates were less than 1 percent of the population, in the range of 0.5 to 0.8 percent. Diagnosis is based on observed behavior and the person's reported experiences.

Genetics, neurobiology, early and current environment, behavioral, social, and experiential components appear to be important contributory factors; some recreational and prescription drugs may cause or worsen symptoms. No single isolated organic cause has been found, but extensive evidence exists for abnormalities in the metabolism of tetrahydrobiopterin (BH4), dopamine, and glutamic acid in people with schizophrenia, psychotic mood disorders, and schizoaffective disorder. People with schizoaffective disorder are likely to have co-occurring conditions, including anxiety disorders and substance use disorder. Social problems such as long-term unemployment, poverty and homelessness are common. The average life expectancy of people with the disorder is shorter than those without it, due to increased physical health problems from an absence of health promoting behaviors such as a sedentary lifestyle, and a higher suicide rate.

The mainstay of current treatment is antipsychotic medication combined with mood stabilizer medication or antidepressant medication, or both. There is growing concern by some researchers that antidepressants may increase psychosis, mania, and long-term mood episode cycling in the disorder. When there is risk to self or others, usually early in treatment, hospitalization may be necessary. Psychiatric rehabilitation, psychotherapy, and vocational rehabilitation are very important for recovery of higher psychosocial function. As a group, people with schizoaffective disorder diagnosed using DSM-IV and criteria have a better outcome than people with schizophrenia, but have variable individual psychosocial functional outcomes compared to people with mood disorders, from worse to the same. Outcomes for people with DSM-5 diagnosed schizoaffective disorder depend on data from prospective cohort studies, which haven't been completed yet.

In DSM-5 and ICD-10, schizoaffective disorder is in the same diagnostic class as schizophrenia, but not in the same class as mood disorders. The diagnosis was introduced in 1933, and its definition was slightly changed in the DSM-5, published in May 2013, because the DSM-IV schizoaffective disorder definition leads to excessive misdiagnosis. The changes made to the schizoaffective disorder definition were intended to make the DSM-5 diagnosis more consistent (or reliable), and to substantially reduce the use of the diagnosis. Additionally, the DSM-5 schizoaffective disorder diagnosis can no longer be used for first episode psychosis.