Although ADHD has most often been treated with medication, medications do not cure ADHD. They are used solely to treat the symptoms associated with this disorder and the symptoms will come back once the medication stops.

Stimulants are typically formulated in fast and slow-acting as well as short and long-acting formulations. The fast-acting amphetamine mixed salts (Adderall) and its derivatives, with short and long-acting formulations bind to the trace amine associated receptor and triggers the release of dopamine into the synaptic cleft. They may have a better cardiovascular disease profile than methylphenidate and potentially better tolerated.

The fast-acting methylphenidate (Ritalin), is a dopamine reuptake inhibitor. In the short term, methylphenidate is well tolerated. However, long term studies have not been conducted in adults and concerns about increases in blood pressure have not been established.

The slow and long-acting nonstimulant atomoxetine (Strattera), is primarily a norepinephrine reuptake inhibitor and, to a lesser extent, a dopamine reuptake inhibitor. It may be more effective for those with predominantly inattentive concentration. It is sometimes prescribed in adults who do not get enough vigilant concentration response from mixed amphetamine salts (Adderall) or get too many side effects. It is also approved for ADHD by the US Food and Drug Administration.

The use of cholinergic adjunctive medications is uncommon and their clinical effects are poorly researched; consequently, cholinergics such as galantamine or varenicline would be off label use for ADHD. New nicotinic cholinergic medications in development for ADHD are pozanicline, ABT-418, and .

Management is based primarily on stopping the usage of the precipitating drugs, the administration of serotonin antagonists such as cyproheptadine, and supportive care including the control of agitation, the control of autonomic instability, and the control of hyperthermia. Additionally, those who ingest large doses of serotonergic agents may benefit from gastrointestinal decontamination with activated charcoal if it can be administered within an hour of overdose. The intensity of therapy depends on the severity of symptoms. If the symptoms are mild, treatment may only consist of discontinuation of the offending medication or medications, offering supportive measures, giving benzodiazepines for myoclonus, and waiting for the symptoms to resolve. Moderate cases should have all thermal and cardiorespiratory abnormalities corrected and can benefit from serotonin antagonists. The serotonin antagonist cyproheptadine is the recommended initial therapy, although there have been no controlled trials demonstrating its efficacy for serotonin syndrome. Despite the absence of controlled trials, there are a number of case reports detailing apparent improvement after people have been administered cyproheptadine. Animal experiments also suggest a benefit from serotonin antagonists. Cyproheptadine is only available as tablets and therefore can only be administered orally or via a nasogastric tube; it is unlikely to be effective in people administered activated charcoal and has limited use in severe cases. Additional pharmacological treatment for severe case includes administering atypical antipsychotic drugs with serotonin antagonist activity such as olanzapine. Critically ill people should receive the above therapies as well as sedation or neuromuscular paralysis. People who have autonomic instability such as low blood pressure require treatment with direct-acting sympathomimetics such as epinephrine, norepinephrine, or phenylephrine. Conversely, hypertension or tachycardia can be treated with short-acting antihypertensive drugs such as nitroprusside or esmolol; longer acting drugs such as propranolol should be avoided as they may lead to hypotension and shock. The cause of serotonin toxicity or accumulation is an important factor in determining the course of treatment. Serotonin is catabolized by monoamine oxidase in the presence of oxygen, so if care is taken to prevent an unsafe spike in body temperature or metabolic acidosis, oxygenation will assist in dispatching the excess serotonin. The same principle applies to alcohol intoxication. In cases of serotonin syndrome caused by monoamine oxidase inhibitors oxygenation will not help to dispatch serotonin. In such instances, hydration is the main concern until the enzyme is regenerated.

Discontinuation syndrome is often prevented by taking medication as directed, and when discontinuing, doing so gradually. When discontinuing an antidepressant with a short half-life, switching to a drug with a longer half-life (e.g. fluoxetine or citalopram) and then discontinuing from that drug can decrease the likelihood and severity of symptoms.

Treatment is dependent on the severity of the discontinuation reaction and whether or not further antidepressant treatment is warranted. In cases where further antidepressant treatment is required then the only step required is restarting the antidepressant; this is usually the case following patient noncompliance with the drug. If antidepressants are no longer required, treatment depends on symptom severity. Mild reactions may only require reassurance. Moderate cases may require symptom management. If symptoms of discontinuation are severe, or do not respond to symptom management, the antidepressant can be reinstated and then withdrawn more cautiously. In rare but severe cases, hospitalization may be required.

Treatment for hyperthermia includes reducing muscle overactivity via sedation with a benzodiazepine. More severe cases may require muscular paralysis with vecuronium, intubation, and artificial ventilation. Suxamethonium is not recommended for muscular paralysis as it may increase the risk of cardiac dysrhythmia from hyperkalemia associated with rhabdomyolysis. Antipyretic agents are not recommended as the increase in body temperature is due to muscular activity, not a hypothalamic temperature set point abnormality.

Treatment is attempted through both cognitive behavioral therapy and psychotropic medication regimens, though the pharmaceutical options have shown limited success. Therapy aids in helping the patient recognize the impulses in hopes of achieving a level of awareness and control of the outbursts, along with treating the emotional stress that accompanies these episodes. Multiple drug regimens are frequently indicated for IED patients. Cognitive Relaxation and Coping Skills Therapy (CRCST) has shown preliminary success in both group and individual settings compared to waitlist control groups. This therapy consists of 12 sessions, the first three focusing on relaxation training, then cognitive restructuring, then exposure therapy. The final sessions focus on resisting aggressive impulses and other preventative measures.

Tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine, fluvoxamine, and sertraline appear to alleviate some pathopsychological symptoms. GABAergic mood stabilizers and anticonvulsive drugs such as gabapentin, lithium, carbamazepine, and divalproex seem to aid in controlling the incidence of outbursts. Anxiolytics help alleviate tension and may help reduce explosive outbursts by increasing the provocative stimulus tolerance threshold, and are especially indicated in patients with comorbid obsessive-compulsive or other anxiety disorders. However, certain anxiolytics are known to "increase" anger and irritability in some individuals, especially benzodiazepines.

No true psychiatric medications are prescribed for factitious disorder. However, selective serotonin reuptake inhibitors (SSRIs) can help manage underlying problems. Medicines such as SSRIs that are used to treat mood disorders can be used to treat FD, as a mood disorder may be the underlying cause of FD. Some authors (such as Prior and Gordon 1997) also report good responses to antipsychotic drugs such as Pimozide. Family therapy can also help. In such therapy, families are helped to better understand patients (the individual in the family with FD) and that person's need for attention.

In this therapeutic setting, the family is urged not to condone or reward the FD individual's behavior. This form of treatment can be unsuccessful if the family is uncooperative or displays signs of denial and/or antisocial disorder. Psychotherapy is another method used to treat the disorder. These sessions should focus on the psychiatrist's establishing and maintaining a relationship with the patient. Such a relationship may help to contain symptoms of FD. Monitoring is also a form that may be indicated for the FD patient's own good; FD (especially proxy) can be detrimental to an individual's health—if they are, in fact, causing true physiological illnesses. Even faked illnesses/injuries can be dangerous, and might be monitored for fear that unnecessary surgery may subsequently be performed.

Treatments for classic (winter-based) seasonal affective disorder include light therapy, medication, ionized-air administration, cognitive-behavioral therapy and carefully timed supplementation of the hormone melatonin.

Photoperiod-related alterations of the duration of melatonin secretion may affect the seasonal mood cycles of SAD. This suggests that light therapy may be an effective treatment for SAD. Light therapy uses a lightbox which emits far more lumens than a customary incandescent lamp. Bright white "full spectrum" light at 10,000 lux, blue light at a wavelength of 480 nm at 2,500 lux or green (actually cyan or blue-green) light at a wavelength of 500 nm at 350 lux are used, with the first-mentioned historically preferred.

Bright light therapy is effective with the patient sitting a prescribed distance, commonly 30–60 cm, in front of the box with her/his eyes open but not staring at the light source for 30–60 minutes. A study published in May 2010 suggests that the blue light often used for SAD treatment should perhaps be replaced by green or white illumination. Discovering the best schedule is essential. One study has shown that up to 69% of patients find lightbox treatment inconvenient and as many as 19% stop use because of this.

Dawn simulation has also proven to be effective; in some studies, there is an 83% better response when compared to other bright light therapy. When compared in a study to negative air ionization, bright light was shown to be 57% effective vs. dawn simulation 50%. Patients using light therapy can experience improvement during the first week, but increased results are evident when continued throughout several weeks. Most studies have found it effective without use year round but rather as a seasonal treatment lasting for several weeks until frequent light exposure is naturally obtained.

Light therapy can also consist of exposure to sunlight, either by spending more time outside or using a computer-controlled heliostat to reflect sunlight into the windows of a home or office. Although light therapy is the leading treatment for seasonal affective disorder, prolonged direct sunlight or artificial lights that don't block the ultraviolet range should be avoided due to the threat of skin cancer.

SSRI (selective serotonin reuptake inhibitor) antidepressants have proven effective in treating SAD. Effective antidepressants are fluoxetine, sertraline, or paroxetine. Both fluoxetine and light therapy are 67% effective in treating SAD according to direct head-to-head trials conducted during the 2006 Can-SAD study. Subjects using the light therapy protocol showed earlier clinical improvement, generally within one week of beginning the clinical treatment. Bupropion extended-release has been shown to prevent SAD for one in eight people, but has not been compared directly to other preventive options in trials.

Negative air ionization, which involves releasing charged particles into the sleep environment, has been found effective with a 47.9% improvement if the negative ions are in sufficient density (quantity).

Depending upon the patient, one treatment (e.g., lightbox) may be used in conjunction with another (e.g., medication).

Modafinil may be an effective and well-tolerated treatment in patients with seasonal affective disorder/winter depression.

Another explanation is that vitamin D levels are too low when people do not get enough Ultraviolet-B on their skin. An alternative to using bright lights is to take vitamin D supplements. However, studies did not show a link between vitamin D levels and depressive symptoms in elderly Chinese nor among elderly British women.

Physical exercise has shown to be an effective form of depression therapy, particularly when in addition to another form of treatment for SAD. One particular study noted marked effectiveness for treatment of depressive symptoms when combining regular exercise with bright light therapy. Patients exposed to exercise which had been added to their treatments in 20 minutes intervals on the aerobic bike during the day along with the same amount of time underneath the UV light were seen to make quick recovery.

Research on treating BDD is limited. Yet anti-depressant medication, such as selective serotonin reuptake inhibitors (SSRIs), and cognitive-behavioral therapy (CBT) are considered effective. SSRIs can help relieve obsessive-compulsive and delusional traits, while cognitive-behavioral therapy can help patients recognize faulty thought patterns. Before treatment, it can help to provide psychoeducation, as with self-help books and support websites.

Symptoms can last for more than 4 weeks and typically resolve within a day of restoring the medication.

Case reports and small randomized studies suggest benzodiazepines, propranolol, and anticholinergics may help treat acute akathisia, but are much less effective in treating chronic akathisia. Taylor et al. found success in lowering the dose of antipsychotic medication as an initial response to drug-induced akathisia, which should be done gradually, if possible. To minimize the risk of akathisia from antipsychotics, the clinician is advised to be conservative when increasing dosages.

One study showed vitamin B to be effective for the treatment of neuroleptic-induced akathisia.

Additional pharmacologic interventions found to have antiakathisia effects (especially for neuroleptic-induced akathisia) include ß-adrenergic antagonists (e.g., propranolol), benzodiazepines (e.g., lorazepam), anticholinergics (e.g., benztropine), and serotonin antagonists (e.g., cyproheptadine) as an alternative.

There are no published or suggested studies on drug treatments for PTED. Selective serotonin reuptake inhibitors (SSRI's) are antidepressants like: Prozac, Paxil, Lexapro, Zoloft, Celexa, and Luvox. They have some benefit in PTED due to their antiobsessional properties. Anafranil, a TCA, is also used extensively.

Pharmaceutical treatments for GAD include selective serotonin reuptake inhibitors (SSRIs). These are the preferred first line of treatment. SSRIs used for this purpose include escitalopram and paroxetine.

Common side effects include nausea, sexual dysfunction, headache, diarrhea, constipation, restlessness, increased risk of suicide in young adults and adolescents, among others. Overdose of an SSRI can result in serotonin syndrome.

Often, apathy is felt after witnessing horrific acts, such as the killing or maiming of people during a war, e.g. posttraumatic stress disorder. It is also known to be a distinct psychiatric syndrome that is associated with many conditions, some of which are: CADASIL syndrome, depression, Alzheimer's disease, Chagas disease, Creutzfeldt–Jakob disease, dementia (and dementias such as Alzheimer's disease, vascular dementia, and frontotemporal dementia), Korsakoff's syndrome, excessive vitamin D, hypothyroidism, hyperthyroidism, general fatigue, Huntington's disease, Pick's disease, progressive supranuclear palsy (PSP), brain damage, schizophrenia, schizoid personality disorder, bipolar disorder, autism, ADHD, Asperger's syndrome, and others. Some medications and the heavy use of drugs such as opiates or GABA-ergic drugs may bring apathy as a side effect.

Benzodiazepines are most often prescribed to people with generalized anxiety disorder. Research suggests that these medications give some relief, at least in the short term. However, they carry some risks, mainly impairment of both cognitive and motor functioning, and psychological and physical dependence that makes it difficult for patients to stop taking them. It has been noted that people taking benzodiazepines are not as alert on their job or at school. Additionally, these medications may impair driving and they are often associated with falls in the elderly, resulting in hip fractures. These shortcomings make the use of benzodiazepines optimal only for short-term relief of anxiety. CBT and medication are of comparable efficacy in the short-term but CBT has advantages over medication in the longer term.

Benzodiazepines (or "benzos") are fast-acting hypnotic sedatives that are also used to treat GAD and other anxiety disorders. Benzodiazepines are prescribed for generalized anxiety disorder and show beneficial effects in the short term. Popular Benzodiazepines for GAD include alprazolam, lorazepam and clonazepam. The World Council of Anxiety does not recommend the long-term use of benzodiazepines because they are associated with the development of tolerance, psychomotor impairment, cognitive and memory impairments, physical dependence and a withdrawal syndrome. Side effects include drowsiness, reduced motor coordination and problems with equilibrioception.

Following a declination or total extinction in response to a previously therapeutic dose of an antidepressant, the issue is clinically addressed as stemming from tolerance development. Several strategies are available, such as exploring drug options from a different drug class used to treat depression. The patient can also choose to switch to another SSRI (or MAOI, if applicable) while maintaining proportionate dose. If tolerance develops in a drug from the same class, the clinician may recommend a regular cycle consisting of all effective treatments within the SSRI or MAOI classes, in order to minimize transitional side effects while maximizing therapeutic efficacy.

Other options include increasing dose of the same medication, or supplementation with another antidepressant. Dual reuptake inhibitors, also known as tricyclic antidepressants have been shown to have lower rates of tachyphylaxis.

MAO inhibitor drugs block an enzyme system resulting in increased stores of monoamine neurotransmitters. More common antidepressants such as tricyclic antidepressants and SSRIs block reuptake transporters causing increased levels of norepinephrine or serotonin in synapses. Mood stabilizers include lithium and many anticonvulsants, such as carbamazepine and lamotrigine are also used for mood disorders. This would demonstrate little to zero cross-tolerance with serotonergic or lithium treatment.

Treatment involves becoming conscious of the addiction through studying, therapy, group work, etc...

Research done by Michel Lejoyeux and Aviv Weinstein suggests that the best possible treatment for CB is through cognitive behavioral therapy. They suggest that a patient first be "evaluated for psychiatric comorbidity, especially with depression, so that appropriate pharmacological treatment can be instituted." Their research indicates that patients who received cognitive behavioral therapy over 10 weeks had reduced episodes of compulsive buying and spent less time shopping as opposed to patients who did not receive this treatment (251).

Lejoyeux and Weinstein also write about pharmacological treatment and studies that question the use of drugs on CB. They declare "Few controlled studies have assessed the effects of pharmacological treatment on compulsive buying, and none have shown any medication to be effective" (252). The most effective treatment is to attend therapy and group work in order to prevent continuation of this addiction.

Selective serotonin reuptake inhibitors such as fluvoxamine and citalopram may be useful in the treatment of CBD, although current evidence is mixed. Opioid antagonists such as naltrexone and nalmefene are promising potential treatments for CBD. A review concluded that evidence is limited and insufficient to support their use at present, however. Naltrexone and nalmefene have also shown effectiveness in the treatment of gambling addiction, an associated disorder.

Orexin-A ( hypocretin-1) has been shown to be strongly wake-promoting in animal models, but unfortunately it does not cross the blood-brain barrier. Therefore, companies have developed orexin receptor antagonists, like suvorexant, for the treatment of insomnia. It is also likely that an orexin-A receptor agonist will be found and developed for the treatment of hypersomnia.

If there is evidence of overdose or it is suspected, the patient should be given gastric lavage, activated charcoal, or both; this could make the difference between life and death in a close situation. It can however aggravate the patient which should be taken into account.

The first line treatments are diazepam and a non-selective beta blocker; other antihypertensive drugs may also be used. It is important to note that not all benzodiazepines and beta blockers are safe to use in an adrenergic storm; for instance, alprazolam and propranolol; alprazolam weakly agonizes dopamine receptors and causes catecholamine release while propranolol mildly promotes some catecholamine release - each worsening the condition.

Adrenergic storms are often idiopathic in nature; however if there is an underlying condition, then that must be addressed after bringing the heart rate and blood pressure down.

Anticholinergic drugs are used to control neuroleptic-induced EPS, although akathisia may require beta blockers or even benzodiazepines. If the EPS are induced by an antipsychotic, EPS may be reduced by dose titration or by switching to an atypical antipsychotic, such as aripiprazole, ziprasidone, quetiapine, olanzapine, risperidone, or clozapine. These medications possess an additional mode of action that is believed to negate their effect on the nigrostriatal pathway, which means they are associated with fewer extrapyramidal side-effects than "conventional" antipsychotics (chlorpromazine, haloperidol, etc.), although some research has shown that second generation neuroleptics cause EPS at the same rate as the first generation drugs.

Commonly used medications for EPS are anticholinergic agents such as benztropine (Cogentin), diphenhydramine (Benadryl), and trihexyphenidyl (Artane). Another common course of treatment includes dopamine agonist agents such as pramipexole. These medications reverse the symptoms of extrapyramidal side effects caused by antipsychotics or other drugs that either directly or indirectly inhibit dopaminergic neurotransmission.

Studies are yet to be undertaken on the optimum dosage of the causative drugs to reduce their side effects (extrapyramidal symptoms (EPS)).

In a test tube model, clarithromycin (an antibiotic approved by the FDA for the treatment of infections) was found to return the function of the GABA system to normal in patients with primary hypersomnias. Investigators therefore treated a few patients with off-label clarithromycin, and most felt their symptoms improved with this treatment. In order to help further determine whether clarithromycin is truly beneficial for the treatment of narcolepsy and idiopathic hypersomnia, a small, double-blind, randomized, controlled clinical trial was completed in 2012. "In this pilot study, clarithromycin improved subjective sleepiness in GABA-related hypersomnia. Larger trials of longer duration are warranted." In 2013, a retrospective review evaluating longer-term clarithromycin use showed efficacy in a large percentage of patients with GABA-related hypersomnia. “It is important to note that the positive effect of clarithromycin is secondary to a benzodiazepine antagonist-like effect, not its antibiotic effects, and treatment must be maintained.”

Amphetamine is a stimulant that has been found to improve both physical and cognitive performance. Amphetamine blocks the reuptake of dopamine and norepinephrine, which delays the onset of fatigue by increasing the amount of dopamine, despite the concurrent increase in norepinephrine, in the central nervous system. Amphetamine is a widely used substance among collegiate athletes for its performance enhancing qualities, as it can improve muscle strength, reaction time, acceleration, anaerobic exercise performance, power output at fixed levels of perceived exertion, and endurance.

Methylphenidate has also been shown to increase exercise performance in time to fatigue and time trial studies.

These drugs block dopamine receptors and some also block serotonin receptors (such as chlorpromazine, the first antipsychotic used clinically). Having been on one or more antipsychotics for any appreciable amount of time results in dramatically reduced sensitivity to others with similar mechanisms of action. However, an antipsychotic with a substantial disparity in pharmacology (e.g. haloperidol and quetiapine) may retain significant efficacy.

Caffeine is the most widely consumed stimulant in North America. In small doses, caffeine can improve endurance. Recently, it has also been shown to delay the onset of fatigue in exercise. The most probable mechanism for the delay of fatigue is through the obstruction of adenosine receptors in the central nervous system. Adenosine is a neurotransmitter that decreases arousal and increases sleepiness. By preventing adenosine from acting, caffeine removes a factor that promotes rest and delays fatigue.