Thought blocking (also known as ), a phenomenon that occurs in people with psychiatric illnesses (usually schizophrenia), occurs when a person's speech is suddenly interrupted by silences that may last a few seconds to a minute or longer. When the person begins speaking again, after the block, they will often speak about a subject unrelated to what was being discussed when blocking occurred. It is described as being experienced as an unanticipated, quick and total emptying of the mind. People with schizophrenia commonly experience thought blocking and may comprehend the experience in peculiar ways. For example a person with schizophrenia might remark that another person has removed their thoughts from their brain.

When doctors diagnose thought blocking, it is important that they consider other causes of pauses in speech and expression, such as petit mal seizures, aphasia, hesitation brought on by anxiety, or slow thought processes. When looking for schizophrenia they may look for thought blocking. It is a common issue with schizophrenia patients.

Psychosis is first and foremost a diagnosis of exclusion. So a new-onset episode of psychosis "cannot" be considered a symptom of a psychiatric disorder until other relevant and known causes of psychosis are properly excluded, or ruled out. Many clinicians improperly perform, or entirely miss this step, introducing avoidable diagnostic error and misdiagnosis.

An initial assessment includes a comprehensive history and physical examination by a physician, psychiatrist, psychiatric nurse practitioner or psychiatric physician assistant. Biological tests should be performed to exclude psychosis associated with or caused by substance use, medication, toxins, surgical complications, or other medical illnesses.

Delirium should be ruled out, which can be distinguished by visual hallucinations, acute onset and fluctuating level of consciousness, indicating other underlying factors, including medical illnesses. Excluding medical illnesses associated with psychosis is performed by using blood tests to measure:

- Thyroid-stimulating hormone to exclude hypo- or hyperthyroidism,

- Basic electrolytes and serum calcium to rule out a metabolic disturbance,

- Full blood count including ESR to rule out a systemic infection or chronic disease, and

- Serology to exclude syphilis or HIV infection.

Other investigations include:

- EEG to exclude epilepsy, and an

- MRI or CT scan of the head to exclude brain lesions.

Because psychosis may be precipitated or exacerbated by common classes of medications, medication-induced psychosis should be ruled out, particularly for first-episode psychosis. Both substance- and medication-induced psychosis can be excluded to a high level of certainty, using a

- Urinalysis and a

- Full serum toxicology screening.

Because some dietary supplements may also induce psychosis or mania, but cannot be ruled out with laboratory tests, a psychotic individual's family, partner, or friends should be asked whether the patient is currently taking any dietary supplements.

Common mistakes made when diagnosing people who are psychotic include:

- Not properly excluding delirium,

- Not appreciating medical abnormalities (e.g., vital signs),

- Not obtaining a medical history and family history,

- Indiscriminate screening without an organizing framework,

- Missing a toxic psychosis by not screening for substances "and" medications

- Not asking family or others about dietary supplements,

- Premature diagnostic closure, and

- Not revisiting or questioning the initial diagnostic impression of primary psychiatric disorder.

Only after relevant and known causes of psychosis are excluded, a mental health clinician may make a psychiatric differential diagnosis using a person's family history, incorporating information from the person with psychosis, and information from family, friends, or significant others.

Types of psychosis in psychiatric disorders may be established by formal rating scales. The Brief Psychiatric Rating Scale (BPRS) assesses the level of 18 symptom constructs of psychosis such as hostility, suspicion, hallucination, and grandiosity. It is based on the clinician's interview with the patient and observations of the patient's behavior over the previous 2–3 days. The patient's family can also answer questions on the behavior report. During the initial assessment and the follow-up, both positive and negative symptoms of psychosis can be assessed using the 30 item Positive and Negative Symptom Scale (PANSS).

Schizophrenia is diagnosed based on criteria in either the American Psychiatric Association's (APA) fifth edition of the "Diagnostic and Statistical Manual of Mental Disorders" (DSM 5), or the World Health Organization's International Statistical Classification of Diseases and Related Health Problems (ICD-10). These criteria use the self-reported experiences of the person and reported abnormalities in behavior, followed by a clinical assessment by a mental health professional. Symptoms associated with schizophrenia occur along a continuum in the population and must reach a certain severity and level of impairment, before a diagnosis is made. As of 2013 there is no objective test.

Medical studies conclude that certain adjunctive drugs effectively palliate the negative symptoms of schizophrenia, mainly alogia. In one study, Maprotiline produced the greatest reduction in alogia symptoms with a 50% decrease in severity. Of the negative symptoms of schizophrenia, alogia had the second best responsiveness to the drugs, surpassed only by attention deficiency. D-amphetamine is another drug that has been tested on people with schizophrenia and found success in alleviating negative symptoms. This treatment, however, has not been developed greatly as it seems to have adverse effects on other aspects of schizophrenia such as increasing the severity of positive symptoms.

In psychiatry, thought withdrawal is the delusional belief that thoughts have been 'taken out' of the patient's mind, and the patient has no power over this. It often accompanies thought blocking. The patient may experience a break in the flow of their thoughts, believing that the missing thoughts have been withdrawn from their mind by some outside agency. This delusion is one of Schneider's first rank symptoms for schizophrenia. Because thought withdrawal is characterized as a delusion, according to the DSM-IV TR it represents a positive symptom of schizophrenia.

In 2013, the American Psychiatric Association released the fifth edition of the DSM (DSM-5). To be diagnosed with schizophrenia, two diagnostic criteria have to be met over much of the time of a period of at least one month, with a significant impact on social or occupational functioning for at least six months. The person had to be suffering from delusions, hallucinations, or disorganized speech. A second symptom could be negative symptoms, or severely disorganized or catatonic behaviour. The definition of schizophrenia remained essentially the same as that specified by the 2000 version of DSM (DSM-IV-TR), but DSM-5 makes a number of changes.

- Subtype classifications – such as catatonic and paranoid schizophrenia – are removed. These were retained in previous revisions largely for reasons of tradition, but had subsequently proved to be of little worth.

- Catatonia is no longer so strongly associated with schizophrenia.

- In describing a person's schizophrenia, it is recommended that a better distinction be made between the current state of the condition and its historical progress, to achieve a clearer overall characterization.

- Special treatment of Schneider's first-rank symptoms is no longer recommended.

- Schizoaffective disorder is better defined to demarcate it more cleanly from schizophrenia.

- An assessment covering eight domains of psychopathology – such as whether hallucination or mania is experienced – is recommended to help clinical decision-making.

The ICD-10 criteria are typically used in European countries, while the DSM criteria are used in the United States and to varying degrees around the world, and are prevailing in research studies. The ICD-10 criteria put more emphasis on Schneiderian first-rank symptoms. In practice, agreement between the two systems is high. The current proposal for the ICD-11 criteria for schizophrenia recommends adding self-disorder as a symptom.

If signs of disturbance are present for more than a month but less than six months, the diagnosis of schizophreniform disorder is applied. Psychotic symptoms lasting less than a month may be diagnosed as brief psychotic disorder, and various conditions may be classed as psychotic disorder not otherwise specified, while schizoaffective disorder is diagnosed if symptoms of mood disorder are substantially present alongside psychotic symptoms. If the psychotic symptoms are the direct physiological result of a general medical condition or a substance, then the diagnosis is one of a psychosis secondary to that condition. Schizophrenia is not diagnosed if symptoms of pervasive developmental disorder are present unless prominent delusions or hallucinations are also present.

Thought disorder (TD) or formal thought disorder (FTD) refers to disorganized thinking as evidenced by disorganized speech. Specific thought disorders include derailment, poverty of speech, tangentiality, illogicality, perseveration, and thought blocking.

Psychiatrists consider formal thought disorder as being one of two types of disordered thinking, with the other type being delusions. The latter involves "content" while the former involves "form". Although the term "thought disorder" can refer to either type, in common parlance it refers most often to a disorder of thought "form" also known as formal thought disorder.

Eugen Bleuler, who named schizophrenia, held that thought disorder was its defining characteristic. However, formal thought disorder is not unique to schizophrenia or psychosis. It is often a symptom of mania, and less often it can be present in other mental disorders such as depression. Clanging or echolalia may be present in Tourette syndrome. Patients with a clouded consciousness, like that found in delirium, also have a formal thought disorder.

However, there is a clinical difference between these two groups. Those with schizophrenia or psychosis are less likely to demonstrate awareness or concern about the disordered thinking. Clayton and Winokur have suggested that this results from a fundamental inability to use the same type of Aristotelian logic as others. On the other hand, patients with a clouded consciousness, referred to as "organic" patients, usually do demonstrate awareness and concern, and complain about being "confused" or "unable to think straight"; Clayton and Winokur suggest that this is because their thought disorder results, instead, from various cognitive deficits.

The concept of thought disorder has been criticized as being based on circular or incoherent definitions. For example, thought disorder is inferred from disordered speech, based on the assumption that disordered speech arises because of disordered thought. Incoherence, or word salad, refers to speech that is unconnected and conveys no meaning to the listener.

Furthermore, although thought disorder is typically associated with psychosis, similar phenomena can appear in different disorders, potentially leading to misdiagnosis—for example, in the case of incomplete yet potentially fruitful thought processes.

It has been suggested that individuals with autism spectrum disorders (ASD) display language disturbances like those found in schizophrenia; a 2008 study found that children and adolescents with ASD showed significantly more illogical thinking and loose associations than control subjects. The illogical thinking was related to cognitive functioning and executive control; the loose associations were related to communication symptoms and to parent reports of stress and anxiety.

The evidence for the effectiveness of early interventions to prevent psychosis appeared inconclusive. Whilst early intervention in those with a psychotic episode might improve short term outcomes, little benefit was seen from these measures after five years. However, there is evidence that cognitive behavioral therapy (CBT) may reduce the risk of becoming psychotic in those at high risk, and in 2014 the UK National Institute for Health and Care Excellence (NICE) recommended preventive CBT for people at risk of psychosis.

In psychology, alogia (Greek ἀ-, “without”, and λόγος, “speech”), or poverty of speech, is a general lack of additional, unprompted content seen in normal speech. As a symptom, it is commonly seen in patients suffering from schizophrenia, and is considered a negative symptom. It can complicate psychotherapy severely because of the considerable difficulty in holding a fluent conversation.

Alogia is often considered a form of aphasia, which is a general impairment in linguistic ability. It often occurs with intellectual disability and dementia as a result of damage to the left hemisphere of the brain. People can revert to alogia as a way of reverse psychology, or avoiding questions.

The long-term outcome for psychotic depression is generally poorer than for non-psychotic depression.

Derealization (sometimes abbreviated as DR) is an alteration in the perception or experience of the external world so that it seems unreal. Other symptoms include feeling as though one's environment is lacking in spontaneity, emotional colouring, and depth. It is a dissociative symptom of many conditions.

Derealization is a subjective experience of unreality of the outside world, while depersonalization is sense of unreality in one's personal self, although most authors currently do not regard derealization (surroundings) and depersonalization (self) as separate constructs.

Chronic derealization may be caused by occipital–temporal dysfunction. These symptoms are common in the population, with a lifetime prevalence of up to 5% and 31–66% at the time of a traumatic event.

Thought insertion is defined by the ICD-10 as feeling as if one's thoughts are not one's own, but rather belong to someone else and have been inserted into one's mind. The person experiencing thought insertion will not necessarily know where the thought is coming from, but is able to distinguish between their own thoughts and those inserted into their minds. However, patients do not experience all thoughts as inserted, only certain ones, normally following a similar content or pattern. This phenomenon is classified as a delusion. A person with this delusional belief is convinced of the veracity of their beliefs and is unwilling to accept such diagnosis.

Thought insertion is a common symptom of psychosis and occurs in many mental disorders and other medical conditions. However, thought insertion is most commonly associated with schizophrenia. Thought insertion, along with thought broadcasting, thought withdrawal, thought blocking and other first rank symptoms, is a primary symptom and should not be confused with the delusional explanation given by the respondent. Although normally associated with some form of psychopathology, thought insertion can also be experienced in those considered nonpathological, usually in spiritual contexts, but also in culturally influenced practices such as mediumship and automatic writing.

Examples of thought insertion:

"She said that sometimes it seemed to be her own thought 'but I don't get the feeling that it is'. She said her 'own thoughts might say the same thing', 'but the feeling isn't the same', 'the feeling is that it is somebody else's'"

"I look out the window and I think that the garden looks nice and the grass looks cool, but the thoughts of Eamonn Andrews come into my mind. There are no other thoughts there, only his. He treats my mind like a screen and flashes thoughts onto it like you flash a picture"

"The subject has thoughts that she thinks are the thoughts of other people, somehow occurring in her own mind. It is not that the subject thinks that other people are making her think certain thoughts as if by hypnosis or psychokinesis, but that other people think the thoughts using the subject's mind as a psychological medium."

Most of the treatments for thought insertion are not specific to the symptom, but rather the symptom is treated through treatment of the psychopathology that causes it. However, one case report considers a way to manage thought insertion through performing thoughts as motor actions of speech. In other words, the patient would speak his thoughts out loud in order to re-give himself the feeling of agency as he could hear himself speaking and then contributing the thought to himself.

Efforts are made to find a treatment which targets the proposed specific underlying pathophysiology of psychotic depression. A promising candidate was mifepristone, which by competitively blocking certain neuro-receptors, renders cortisol less able to directly act on the brain and was thought to therefore correct an overactive HPA axis. However, a Phase III clinical trial, which investigated the use of mifepristone in PMD, was terminated early due to lack of efficacy.

Transcranial magnetic stimulation (TMS) is being investigated as an alternative to ECT in the treatment of depression. TMS involves the administration of a focused electromagnetic field to the cortex to stimulate specific nerve pathways.

Research has shown that psychotic depression differs from non-psychotic depression in a number of ways: potential precipitating factors, underlying biology, symptomatology beyond psychotic symptoms, long-term prognosis, and responsiveness to psychopharmacological treatment and ECT.

Derealization can accompany the neurological conditions of epilepsy (particularly temporal lobe epilepsy), migraine, and mild head injury. There is a similarity between visual hypo-emotionality, a reduced emotional response to viewed objects, and derealization. This suggests a disruption of the process by which perception becomes emotionally coloured. This qualitative change in the experiencing of perception may lead to reports of anything viewed being unreal or detached.

Derealization can also manifest as an indirect result of certain vestibular disorders such as labyrinthitis. This is thought to result from the experience of anxiety precipitated by the functional disparity that arises between the ability to reconcile external stimuli relative to motion and equilibrioception that are compromised by vestibular dysfunction with the internal perceptions and expectations regarding the physical environment.

An alternative explanation holds that a possible effect of vestibular dysfunction includes responses in the form of the modulation of noradrenergic and serotonergic activity due to a misattribution of vestibular symptoms to the presence of imminent physical danger resulting in the experience of anxiety or panic, which subsequently generate feelings of derealization.

Cannabis, psychedelics, dissociatives, antidepressants, caffeine, nitrous oxide, albuterol, and nicotine can all produce feelings resembling derealization, particularly when taken in excess. It can result from alcohol withdrawal or benzodiazepine withdrawal. Opiate withdrawal can also cause feelings of derealization.

Derealization can also be a symptom of severe sleep disorders and mental disorders like depersonalization disorder, borderline personality disorder, bipolar disorder, schizophrenia, dissociative identity disorder, and anxiety disorders.

Interoceptive exposure can be used as a means to induce derealization, as well as the related phenomenon depersonalization.

The prognosis is best when identified early and treated aggressively. In these cases NMS is not usually fatal. In previous studies the mortality rates from NMS have ranged from 20%–38%; however, in the last two decades, mortality rates have fallen below 10% due to early recognition and improved management. Re-introduction to the drug that originally caused NMS to develop may also trigger a recurrence, although in most cases it does not.

Memory impairment is a consistent feature of recovery from NMS, and usually temporary, though in some cases, may become persistent.

As sexual anhedonia is the source of considerable dissatisfaction among its sufferers, several treatment methods have been devised to help patients cope. Exploration of psychological factors is one method, which includes exploring past trauma, abuse, and prohibitions in the cultural and religious history of the person. Sex therapy might also be used as a way of helping a sufferer realign and examine his or her expectations of an orgasm. Contributing medical causes must also be ruled out and medications might have to be switched when appropriate. Additionally, blood testing might help determine levels of hormones and other things in the bloodstream that might inhibit pleasure. This condition can also be treated with drugs that increase dopamine, such as oxytocin, along with other drugs. In general, it is recommended that a combination of psychological and physiological treatments should be used to treat the disorder.

Other drugs which may be helpful in the treatment of this condition include dopamine agonists, oxytocin, phosphodiesterase type 5 inhibitors, and alpha-2 receptor blockers like yohimbine.

Differentiating NMS from other neurological disorders can be very difficult. It requires expert judgement to separate symptoms of NMS from other diseases. Some of the most commonly mistaken diseases are encephalitis, toxic encephalopathy, status epilepticus, heat stroke, and malignant hyperthermia. Due to the comparative rarity of NMS, it is often overlooked and immediate treatment for the syndrome is delayed. Drugs such as cocaine and amphetamine may also produce similar symptoms.

The differential diagnosis is similar to that of hyperthermia, and includes serotonin syndrome. Features which distinguish NMS from serotonin syndrome include bradykinesia, muscle rigidity, and a high white blood cell count.

Sexual anhedonia, also known as pleasure dissociative orgasmic disorder, is a condition in which an individual cannot feel pleasure from an orgasm. It is thought to be a variant of hypoactive sexual desire disorder.

Several treatment methods are available to help prevent CINV. Pharmaceutical treatment is generally separated into two types: prophylactic (preventative) treatment, given before the dose of chemotherapy agents, and rescue treatment, given to treat breakthrough nausea and vomiting.

In the past, the prognosis for patients with this disease had been very poor; with many patients suffering from severe disability or death. Now, patients are responding remarkably well to current treatments and the majority of patients go into spontaneous remission. For those that do not go into remission, the symptoms of hemiballismus can generally be very well controlled with medication.

Due to the rarity of this disorder, scientists know very little about the details of hemiballismus. There are still many unanswered questions such as:

•There appears to be a discrepancy between this disorder in humans and animals that has yet to be explained.

•Hemiballismus can also be induced by damage to other areas of the basal ganglia besides the subthalamic nucleus. Why is this? Research is being done in these areas in order to give scientists and clinicians a better model for this disease that will ultimately lead to better diagnosis and treatment of this disorder.

•Research is also being done on why certain treatments seem to help hemiballistic patients when they should seemingly do more harm. An example of this is why lesioning the globus pallidus seems to reduce hemiballistic movements.

•Why does blocking dopamine help reduce patients’ symptoms?

Olanzapine, as well as several other neuroleptic drugs, have also has been investigated for the control of CINV. A 2007 study demonstrated Olanzapine's successful potential for this use, achieving a complete response in the acute prevention of nausea and vomiting in 100% of patients treated with moderately and highly emetogenic chemotherapy, when used in combination with palonosetron and dexamethasone. Neuroleptic agents are now indicated for rescue treatment and the control of breakthrough nausea and vomiting.

Some studies and patient groups say that the use of cannabinoids derived from cannabis during chemotherapy greatly reduces the associated nausea and vomiting, and enables the patient to eat. Synthesized tetrahydrocannabinol (also one of the main active substances in marijuana) is marketed as Marinol and may be practical for this application. Natural medical cannabis is also used and recommended by some oncologists, though its use is regulated and it is not legal in all jurisdictions. However, Marinol was less effective than megestrol acetate in helping cancer patients regain lost appetites. A phase III study found no difference in effects of an oral cannabis extract or THC on appetite and quality of life (QOL) in patients with cancer-related anorexia-cachexia syndrome (CACS) to placebo.

Dexamethasone, a corticosteroid, is often used alongside other antiemetic drugs, as it has synergistic action with many of them, although its specific antiemetic mechanism of action is not fully understood. Metoclopramide, a dopamine D receptor antagonist with possible other mechanisms, is an older drug that is sometimes used, either on its own or in combination with others. Histamine blockers such as diphenhydramine or meclozine may be used in rescue treatment. Lorazepam and diazepam may sometimes be used to relieve anxiety associated with CINV before administration of chemotherapy, and are also often used in the case of rescue treatment.

When treating hemiballismus, it is first important to treat whatever may be causing the manifestation of this disorder. This could be hyperglycemia, infections, or neoplastic lesions. Some patients may not even need treatment because the disorder is not severe and can be self – limited.

Dopamine Blockers

When pharmacological treatment is necessary, the most standard type of drug to use is an antidopaminergic drug. Blocking dopamine is effective in about ninety percent of patients. Perphenazine, pimozide, haloperidol, and chlorpromazine are standard choices for treatment. Scientists are still unsure as to why this form of treatment works, as dopamine has not been directly linked to hemiballismus.

Anticonvulsants

An anticonvulsant called topiramate has helped patients in three cases and may be a viable treatment for the future.

ITB Therapy

Intrathecal baclofen (ITB) therapy is used to treat a variety of movement disorders such as cerebral palsy and multiple sclerosis. It can also be a possibility to help treat hemiballismus. In one case, before ITB the patient had an average of 10-12 ballism episodes of the right lower limb per hour. During episodes, the right hip would flex up to about 90 degrees, with a fully extended knee. After an ITB pump was implanted and the correct dosage was found, the frequency of ballistic right leg movements decreased to about three per day, and the right hip flexed to only 30 degrees. The patient was also able to better isolate individual distal joint movements in the right lower limb. The patient currently receives 202.4 microg/day of ITB and continues to benefit almost 6 years after the ITB pump was implanted.

Botulinum Injections

New uses for botulinum toxin have included treatment of hemiballismus. However, this is still in the early stages of testing. This treatment deals with the muscular manifestations of hemiballismus as opposed to the neurological causes.

Tetrabenazine

Tetrabenazine has been used to treat other movement disorders, but is now being used to treat hemiballismus. Patients using this medication have had a dramatic response. However, lowering the dosage leads to a return of symptoms. This drug works by depleting dopamine.

Antipsychotics

In one case, a patient had not been responding to haloperidol, thus the physician tried olanzapine. The patient made a significant recovery. More research is being performed on the use of these types of drugs in treating hemiballismus.

Functional Neurosurgery

Surgery as a treatment should only be used on patients with severe hemiballismus that has not responded to treatment. Lesioning of the globus pallidus or deep brain stimulation of the globus pallidus are procedures that can be used on humans. Usually, lesioning is favored over deep brain stimulation because of the maintenance required to continue stimulating the brain correctly and effectively.

Initial screening for CIP/CIM may be performed using an objective scoring system for muscle strength. The Medical Research Council (MRC) score is one such tool, and sometimes used to help identify CIP/CIM patients in research studies. The MRC score involves assessing strength in 3 muscle groups in the right and left sides of both the upper and lower extremities. Each muscle tested is given a score of 0-5, giving a total possible score of 60. An MRC score less than 48 is suggestive of CIP/CIM. However, the tool requires that patients be awake and cooperative, which is often not the case. Also, the screening tool is non-specific, because it does not identify the cause a person's muscle weakness.

Once weakness is detected, the evaluation of muscle strength should be repeated several times. If the weakness persists, then a muscle biopsy, a nerve conduction study (electrophysiological studies), or both should be performed.