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.

Several treatment guidelines recommend either the combination of a second-generation antidepressant and atypical antipsychotic or tricyclic antidepressant monotherapy or electroconvulsive therapy (ECT) as the first-line treatment for unipolar psychotic depression.

Pharmaceutical treatments can include tricyclic antidepressants, atypical antipsychotics, or a combination of an antidepressant from the newer, more well tolerated SSRI or SNRI categories and an atypical antipsychotic. Olanzapine may be an effective monotherapy in psychotic depression, although there is evidence that it is ineffective for depressive symptoms as a monotherapy; and olanzapine/fluoxetine is more effective. Quetiapine monotherapy may be particularly helpful in psychotic depression since it has both antidepressant and antipsychotic effects and a reasonable tolerability profile compared to other atypical antipsychotics. The current drug-based treatments of psychotic depression are reasonably effective but can cause side effects, such as nausea, headaches, dizziness, and weight gain. Tricyclic antidepressants are particularly dangerous in overdose due to their potential to cause potentially-fatal cardiac arrhythmias.

In the context of psychotic depression, the following are the most well-studied antidepressant/antipsychotic combinations

"First-generation"

- Amitriptyline/perphenazine

- Amitriptyline/haloperidol

"Second-generation"

- Venlafaxine/quetiapine?

- Olanzapine/fluoxetine

- Olanzapine/sertraline

In modern practice of ECT a therapeutic clonic seizure is induced by electric current via electrodes placed on an anaesthetised, unconscious patient. Despite much research the exact mechanism of action of ECT is still not known. ECT carries the risk of temporary cognitive deficits (e.g., confusion, memory problems), in addition to the burden of repeated exposures to general anesthesia.

The first-line psychiatric treatment for schizophrenia is antipsychotic medication, which can reduce the positive symptoms of psychosis in about 7 to 14 days. Antipsychotics, however, fail to significantly improve the negative symptoms and cognitive dysfunction. In those on antipsychotics, continued use decreases the risk of relapse. There is little evidence regarding effects from their use beyond two or three years. However use of anti-psychotics can lead to dopamine hypersensitivity increasing the risk of symptoms if antipsychotics are stopped.

The choice of which antipsychotic to use is based on benefits, risks, and costs. It is debatable whether, as a class, typical or atypical antipsychotics are better. Amisulpride, olanzapine, risperidone, and clozapine may be more effective but are associated with greater side effects. Typical antipsychotics have equal drop-out and symptom relapse rates to atypicals when used at low to moderate dosages. There is a good response in 40–50%, a partial response in 30–40%, and treatment resistance (failure of symptoms to respond satisfactorily after six weeks to two or three different antipsychotics) in 20% of people. Clozapine is an effective treatment for those who respond poorly to other drugs ("treatment-resistant" or "refractory" schizophrenia), but it has the potentially serious side effect of agranulocytosis (lowered white blood cell count) in less than 4% of people.

Most people on antipsychotics have side effects. People on typical antipsychotics tend to have a higher rate of extrapyramidal side effects, while some atypicals are associated with considerable weight gain, diabetes and risk of metabolic syndrome; this is most pronounced with olanzapine, while risperidone and quetiapine are also associated with weight gain. Risperidone has a similar rate of extrapyramidal symptoms to haloperidol. It remains unclear whether the newer antipsychotics reduce the chances of developing neuroleptic malignant syndrome or tardive dyskinesia, a rare but serious neurological disorder.

For people who are unwilling or unable to take medication regularly, long-acting depot preparations of antipsychotics may be used to achieve control. They reduce the risk of relapse to a greater degree than oral medications. When used in combination with psychosocial interventions, they may improve long-term adherence to treatment. The American Psychiatric Association suggests considering stopping antipsychotics in some people if there are no symptoms for more than a year.

A number of psychosocial interventions may be useful in the treatment of schizophrenia including: family therapy, assertive community treatment, supported employment, cognitive remediation, skills training, token economic interventions, and psychosocial interventions for substance use and weight management. Family therapy or education, which addresses the whole family system of an individual, may reduce relapses and hospitalizations. Evidence for the effectiveness of cognitive-behavioral therapy (CBT) in either reducing symptoms or preventing relapse is minimal. Evidence for metacognitive training is mixed with one 2016 review finding benefit and another not. Art or drama therapy have not been well-researched.

The treatment of psychosis depends on the specific diagnosis (such as schizophrenia, bipolar disorder or substance intoxication). The first-line psychiatric treatment for many psychotic disorders is antipsychotic medication, which can reduce the positive symptoms of psychosis in about 7 to 14 days.

The choice of which antipsychotic to use is based on benefits, risks, and costs. It is debatable whether, as a class, typical or atypical antipsychotics are better. Tentative evidence supports that amisulpride, olanzapine, risperidone and clozapine may be more effective for positive symptoms but result in more side effects. Typical antipsychotics have equal drop-out and symptom relapse rates to atypicals when used at low to moderate dosages. There is a good response in 40–50%, a partial response in 30–40%, and treatment resistance (failure of symptoms to respond satisfactorily after six weeks to two or three different antipsychotics) in 20% of people. Clozapine is an effective treatment for those who respond poorly to other drugs ("treatment-resistant" or "refractory" schizophrenia), but it has the potentially serious side effect of agranulocytosis (lowered white blood cell count) in less than 4% of people.

Most people on antipsychotics get side effects. People on typical antipsychotics tend to have a higher rate of extrapyramidal side effects while some atypicals are associated with considerable weight gain, diabetes and risk of metabolic syndrome; this is most pronounced with olanzapine, while risperidone and quetiapine are also associated with weight gain. Risperidone has a similar rate of extrapyramidal symptoms to haloperidol.

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.

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.

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.

5-HT receptor antagonists are very effective antiemetics and constitute a great advance in the management of CINV. These drugs block one or more of the nerve signals that cause nausea and vomiting. During the first 24 hours after chemotherapy, the most effective approach appears to be blocking the 5-HT nerve signal. Approved 5-HT inhibitors include dolasetron (Anzemet), granisetron (Kytril, Sancuso), and ondansetron (Zofran). Their antiemetic effect due to blockade of 5HT3 receptor on vagal afferent in the gut. in addition they also block 5-HT3 receptors in CTZ and STN. The newest 5-HT inhibitor, palonosetron (Aloxi), also prevents delayed nausea and vomiting, which can occur during the 2–5 days after treatment. Since some patients have trouble swallowing pills, these drugs are often available by injection, as orally disintegrating tablets, or as transdermal patches.

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.

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.

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.

Alogia can be brought on by frontostriatal dysfunction which causes degradation of the semantic store, the center located in the temporal lobe that processes meaning in language. A subgroup of chronic schizophrenia patients in a word generation experiment generated fewer words than the unaffected subjects and had limited lexicons, evidence of the weakening of the semantic store. Another study found that when given the task of naming items in a category, schizophrenia patients displayed a great struggle but improved significantly when experimenters employed a second stimulus to guide behavior unconsciously. This conclusion was similar to results produced from patients with Huntington's and Parkinson's disease, ailments which also involve frontostriatal dysfunction.

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.

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.

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.

NMS is a medical emergency and can lead to death if untreated. The first step is to stop the antipsychotic medication and treat the hyperthermia aggressively, such as with cooling blankets or ice packs to the axillae and groin. Supportive care in an intensive care unit capable of circulatory and ventilatory support is crucial. The best pharmacological treatment is still unclear. Dantrolene has been used when needed to reduce muscle rigidity, and more recently dopamine pathway medications such as bromocriptine have shown benefit.

Amantadine is another treatment option due to its dopaminergic and anticholinergic effects.

Apomorphine may be used however its use is supported by little evidence. Benzodiazepines may be used to control . Highly elevated blood myoglobin levels can result in kidney damage, therefore aggressive intravenous hydration with diuresis may be required. When recognized early NMS can be successfully managed; however, up to 10% of cases can be fatal.

Should a patient subsequently require an antipsychotic, trialing a low dose of a low-potency atypical antipsychotic is recommended.

Before prescribing medication for these conditions which often resolve spontaneously, recommendations have pointed to improved skin hygiene, good hydration via fluids, good nutrition, and installation of padded bed rails with use of proper mattresses. Pharmacological treatments include the typical neuroleptic agents such as fluphenazine, pimozide, haloperidol and perphenazine which block dopamine receptors; these are the first line of treatment for hemiballismus. Quetiapine, sulpiride and olanzapine, the atypical neuroleptic agents, are less likely to yield drug-induced parkinsonism and tardive dyskinesia. Tetrabenazine works by depleting presynaptic dopamine and blocking postsynaptic dopamine receptors, while reserpine depletes the presynaptic catecholamine and serotonin stores; both of these drugs treat hemiballismus successfully but may cause depression, hypotension and parkinsonism. Sodium valproate and clonazepam have been successful in a limited number of cases. Stereotactic ventral intermediate thalamotomy and use of a thalamic stimulator have been shown to be effective in treating these conditions.

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.

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 medical treatment of essential tremor at the Movement Disorders Clinic at Baylor College of Medicine begins with minimizing stress and tremorgenic drugs along with recommending a restricted intake of beverages containing caffeine as a precaution, although caffeine has not been shown to significantly intensify the presentation of essential tremor. Alcohol amounting to a blood concentration of only 0.3% has been shown to reduce the amplitude of essential tremor in two-thirds of patients; for this reason it may be used as a prophylactic treatment before events during which one would be embarrassed by the tremor presenting itself. Using alcohol regularly and/or in excess to treat tremors is highly unadvisable, as there is a purported correlation between tremor and alcoholism. Alcohol is thought to stabilize neuronal membranes via potentiation of GABA receptor-mediated chloride influx. It has been demonstrated in essential tremor animal models that the food additive 1-octanol suppresses tremors induced by harmaline, and decreases the amplitude of essential tremor for about 90 minutes.

Two of the most valuable drug treatments for essential tremor are propranolol, a beta blocker, and primidone, an anticonvulsant. Propranolol is much more effective for hand tremor than head and voice tremor. Some beta-adrenergic blockers (beta blockers) are not lipid-soluble and therefore cannot cross the blood–brain barrier (propranolol being an exception), but can still act against tremors; this indicates that this drug’s mechanism of therapy may be influenced by peripheral beta-adrenergic receptors. Primidone’s mechanism of tremor prevention has been shown significantly in controlled clinical studies. The benzodiazepine drugs such as diazepam and barbiturates have been shown to reduce presentation of several types of tremor, including the essential variety. Controlled clinical trials of gabapentin yielded mixed results in efficacy against essential tremor while topiramate was shown to be effective in a larger double-blind controlled study, resulting in both lower Fahn-Tolosa-Marin tremor scale ratings and better function and disability as compared to placebo.

It has been shown in two double-blind controlled studies that injection of botulinum toxin into muscles used to produce oscillatory movements of essential tremors, such as forearm, wrist and finger flexors, may decrease the amplitude of hand tremor for approximately three months and that injections of the toxin may reduce essential tremor presenting in the head and voice. The toxin also may help tremor causing difficulty in writing, although properly adapted writing devices may be more efficient. Due to high incidence of side effects, use of botulinum toxin has only received a C level of support from the scientific community.

Deep brain stimulation toward the ventral intermediate nucleus of the thalamus and potentially the subthalamic nucleus and caudal zona incerta nucleus have been shown to reduce tremor in numerous studies. That toward the ventral intermediate nucleus of the thalamus has been shown to reduce contralateral and some ipsilateral tremor along with tremors of the cerebellar outflow, head, resting state and those related to hand tasks; however, the treatment has been shown to induce difficulty articulating thoughts (dysarthria), and loss of coordination and balance in long-term studies. Motor cortex stimulation is another option shown to be viable in numerous clinical trials.

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."

Many drugs used to treat myoclonus dystonia do not have a significant impact individually, but when combined, can work on different brain mechanisms to best alleviate symptoms. The method of treatment used depends on the severity of the symptoms presented in the individual, and whether the underlying cause of the syndrome is known.

Anticholinergics like benzatropine alleviate dystonia symptoms by blocking reuptake of acetylcholine. Acetylcholine is involved in the pathophysiology of dystonia within the basal ganglia, although its exact role has not been determined. Acetylcholine is involved with dopamine and glutamate pathways in the basal ganglia, in addition to presynaptic muscarinic receptors which are involved in motor control. Acetylcholine is usually overactive in dystonia patients and blocking of this neurotransmitter would reduce contortion of the upper body, but can produce side effects of drowsiness, confusion and memory issues in adults.