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 .

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.

Dietary modifications may be of benefit to a small proportion of children with ADHD. A 2013 meta-analysis found less than a third of children with ADHD see some improvement in symptoms with free fatty acid supplementation or decreased eating of artificial food coloring. These benefits may be limited to children with food sensitivities or those who are simultaneously being treated with ADHD medications. This review also found that evidence does not support removing other foods from the diet to treat ADHD. A 2014 review found that an elimination diet results in a small overall benefit. A 2016 review stated that the use of a gluten-free diet as standard ADHD treatment is discouraged. Iron, magnesium and iodine may also have an effect on ADHD symptoms. There is a small amount of evidence that lower tissue zinc levels may be associated with ADHD. In the absence of a demonstrated zinc deficiency (which is rare outside of developing countries), zinc supplementation is not recommended as treatment for ADHD. However, zinc supplementation may reduce the minimum effective dose of amphetamine when it is used with amphetamine for the treatment of ADHD. There is evidence of a modest benefit of omega 3 fatty acid supplementation, but it is not recommended in place of traditional medication.

Treatment of SCT has not been well investigated. Initial drug studies were done only with the ADHD medication, methylphenidate (Ritalin/Concerta), and even then only with children who were diagnosed as ADD without hyperactivity (DSM-III) and not specifically for SCT. The research seems to have found that most children with DSM-III ADD-H (currently ADHD-C) responded well at medium-to-high doses. However, a sizable percentage of children with ADD without hyperactivity (using DSM-III criteria; therefore the results may apply to SCT) did not gain much benefit from methylphenidate, and when they did benefit, it was at a much lower dose.

However, one study and a retrospective analysis of medical histories found that the presence or absence of SCT symptoms made no difference in response to methylphenidate in children with ADHD-I. But these studies did not specifically and explicitly examine the effect of the drug on SCT symptoms in children. The only medication study to date who did this used atomoxetine (Strattera) and found it to have significant beneficial effects that were independent of ADHD symptoms.

Only one study has investigated the use of behavior modification methods at home and school for children with predominantly SCT symptoms and it found good success.

In April 2014, "The New York Times" reported that sluggish cognitive tempo is the subject of pharmaceutical company clinical drug trials, including ones by Eli Lilly that proposed that one of its biggest-selling drugs, Strattera, could be prescribed to treat proposed symptoms of sluggish cognitive tempo. Other researchers believe that there is no effective treatment for SCT.

Stimulant medications are the pharmaceutical treatment of choice. They have at least some effect on symptoms in the short term in about 80% of people. Methylphenidate appears to improve symptoms as reported by teachers and parents. Stimulants may also reduce the risk of unintentional injuries in children with ADHD.

There are a number of non-stimulant medications, such as atomoxetine, bupropion, guanfacine, and clonidine that may be used as alternatives, or added to stimulant therapy. There are no good studies comparing the various medications; however, they appear more or less equal with respect to side effects. Stimulants appear to improve academic performance while atomoxetine does not. Atomoxetine, due to its lack of addiction liability, may be preferred in those who are at risk of recreational or compulsive stimulant use. There is little evidence on the effects of medication on social behaviors. , the long-term effects of ADHD medication have yet to be fully determined. Magnetic resonance imaging studies suggest that long-term treatment with amphetamine or methylphenidate decreases abnormalities in brain structure and function found in subjects with ADHD.

Guidelines on when to use medications vary by country, with the United Kingdom's National Institute for Health and Care Excellence recommending use for children only in severe cases, though for adults medication is a first-line treatment, while most United States guidelines recommend medications in most age groups. Medications are not recommended for preschool children. Underdosing of stimulants may occur and result in a lack of response or later loss of effectiveness. This is particularly common in adolescents and adults as approved dosing is based on school-aged children, causing some practitioners to use weight based or benefit based off-label dosing instead.

While stimulants and atomoxetine are usually safe, there are side-effects and contraindications to their use. A large overdose on ADHD stimulants is commonly associated with symptoms such as stimulant psychosis and mania; although very rare, at therapeutic doses these events appear to occur in approximately 0.1% of individuals within the first several weeks after starting amphetamine or methylphenidate therapy. Administration of an antipsychotic medication has been found to effectively resolve the symptoms of acute amphetamine psychosis. Regular monitoring has been recommended in those on long-term treatment. Stimulant therapy should be stopped periodically to assess continuing need for medication, decrease possible growth delay, and reduce tolerance. Long-term misuse of stimulant medications at doses above the therapeutic range for ADHD treatment is associated with addiction and dependence. Untreated ADHD, however, is also associated with elevated risk of substance use disorders and conduct disorders. The use of stimulants appears to either reduce this risk or have no effect on it. The safety of these medications in pregnancy is unclear.

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.

Before delirium treatment, the cause must be established. Medication such as antipsychotics or benzodiazepines can help reduce the symptoms for some cases. For alcohol or malnourished cases, vitamin B supplements are recommended and for extreme cases, life-support can be used.

Reactive strategies include:

- Redirection: distracting the person by offering another activity, or changing the topic of conversation. Offer the person a choice of 2 or 3 things, but no more than 3, because this can be overwhelming. In offering a choice, make sure to pause to allow the person time to process the information and give a response.

- Talking to the person and finding out what the problem is

- Working out what the person's behaviour is trying to communicate

- Crisis management

Cognitive-behavioural therapy (CBT) is a frequently suggested treatment for executive dysfunction, but has shown limited effectiveness. However, a study of CBT in a group rehabilitation setting showed a significant increase in positive treatment outcome compared with individual therapy. Patients' self-reported symptoms on 16 different ADHD/executive-related items were reduced following the treatment period.

There is no cure for neurocognitive disorder or the diseases that cause it. Antidepressants, antipsychotics, and other medications that treat memory loss and behavioral symptoms are available and may help to treat the diseases. Ongoing psychotherapy and psychosocial support for patients and families are usually necessary for clear understanding and proper management of the disorder and to maintain a better quality of life for everyone involved. Speech therapy has been shown to help with language impairment.

Studies suggest that diets with high Omega 3 content, low in saturated fats and sugars, along with regular exercise can increase the level of brain plasticity. Other studies have shown that mental exercise such a newly developed “computerized brain training programs” can also help build and maintain targeted specific areas of the brain. These studies have been very successful for those diagnosed with schizophrenia and can improve fluid intelligence, the ability to adapt and deal with new problems or challenges the first time encountered, and in young people, it can still be effective in later life.

A person with amnesia may slowly be able to recall their memories or work with an occupational therapist to learn new information to replace what was lost, or to use intact memories as a basis for taking in new information. If it is caused by an underlying cause such as Alzheimer's disease or infections, the cause may be treated but the amnesia may not be.

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.

Positive Behaviour Support (PBS) is a treatment approach that looks at the best way to work with each individual with disabilities. A behavioural therapist conducts a functional analysis of behaviour which helps to determine ways to improve the quality of life for the person and does not just deal with problem behaviour.

PBS also acknowledges the needs of support staff and includes strategies to manage crises when they arise. The following model is a brief guide to staff to remind them of key things to think about when planning support for a person with disabilities. There are two main objectives: reacting situationally when the behaviour occurs, and then acting proactively to prevent the behaviour from occurring.

An international review of psychiatrists' management of patients with generalized anxiety disorder (GAD) reported that the preferred first-line pharmacological treatments of GAD were selective serotonin reuptake inhibitors (SSRIs) (80%), followed by serotonin–norepinephrine reuptake inhibitors (SNRIs) (43%), and pregabalin (35%). Preferred second-line treatments were SNRIs (41%) and pregabalin (36%).

The current treatments for CCAS focus on relieving the symptoms. One treatment is a cognitive-behavioral therapy (CBT) technique that involves making the patient aware of his or hers cognitive problems. For example, many CCAS patients struggle with multitasking. With CBT, the patient would have to be aware of this problem and focus on just one task at a time. This technique is also used to relieve some motor symptoms. In a case study with a patient who had a stroke and developed CCAS, improvements in mental function and attention were achieved through reality orientation therapy and attention process training. Reality orientation therapy consists of continually exposing the patient to stimuli of past events, such as photos. Attention process training consists of visual and auditory tasks that have been shown to improve attention. The patient struggled in applying these skills to “real-life” situations. It was the help of his family at home that significantly helped him regain his ability to perform activities of daily living. The family would motivate the patient to perform basic tasks and made a regular schedule for him to follow.

Transcranial magnetic stimulation (TMS) has also been proposed to be a possible treatment of psychiatric disorders of the cerebellum. One study used TMS on the vermis of patients with schizophrenia. After stimulation, the patients showed increased happiness, alertness and energy, and decreased sadness. Neuropsychological testing post-stimulation showed improvements in working memory, attention, and visual spatial skill. Another possible method of treatment for CCAS is doing exercises that are used to relieve the motor symptoms. These physical exercises have been shown to also help with the cognitive symptoms.

Medications that help relieve deficits in traumatic brain injuries in adults have been proposed as candidates to treat CCAS. Bromocriptine, a direct D2 agonist, has been shown to help with deficits in executive function and spatial learning abilities. Methylphendiate has been shown to help with deficits in attention and inhibition. Neither of these drugs has yet been tested on a CCAS population. It may also be that some of the symptoms of CCAS improve over time without any formal treatment. In the original report of CCAS, four patients with CCAS were re-examined one to nine months after their initial neuropsychological evaluation. Three of the patients showed improvement in deficits without any kind of formal treatment, though executive function was still found to be one standard deviation below average. In one patient, the deficits worsened over time. This patient had cerebellar atrophy and worsened in visual spatial abilities, concept formation, and verbal memory. It should be noted that none of these treatments were tested on a large enough sample to determine if they would help with the general CCAS population. Further research needs to be done on treatments for CCAS.

The prognosis of SCT is unknown. In contrast, much is known about the adolescent and adult outcomes of children having ADHD. Those with SCT symptoms typically show a later onset of their symptoms than do those with ADHD, perhaps by as much as a year or two later on average. They have as much or more difficulty with academic tasks and far fewer social difficulties than do people having ADHD. They do not have the same risks for oppositional defiant disorder, conduct disorder, or social aggression and thus may have different life course outcomes compared to children with ADHD-HI and Combined subtypes who have far higher risks for these other "externalizing" disorders.

However, unlike ADHD, there are no longitudinal studies of children with SCT that can shed light on the developmental course and adolescent or adult outcomes of these individuals.

There is much research that needs to be conducted on CCAS. A necessity for future research is to conduct more longitudinal studies in order to determine the long-term effects of CCAS. One way this can be done is by studying cerebellar hemorrhage that occurs during infancy. This would allow CCAS to be studied over a long period to see how CCAS affects development. It may be of interest to researchers to conduct more research on children with CCAS, as the survival rate of children with tumors in the cerebellum is increasing. Hopefully future research will bring new insights on CCAS and develop better treatments.

Aside from discontinuation of glucocorticoid medication, potential treatments discussed in the research literature include:

- anti-glucocorticoids

- psychoactive drugs that up-regulate the GRII glucocorticoid receptor:

- tricyclic antidepressants: Desipramine, Imipramine, and Amitriptyline (SSRIs do not )

- serotonin antagonists: Ketanserin

- mood stabilizers: Lithium

- corticotropin-releasing hormone (CRH) antagonists

- glutamate antagonists

- dehydroepiandrosterone (DHEA)

- small molecule brain-derived neurotrophic factor (BDNF) analogs

- stress reduction therapies and exercise.

Since 1997 there has been experimental and clinical practice of psychosocial treatment for adults with executive dysfunction, and particularly attention-deficit/hyperactivity disorder (ADHD). Psychosocial treatment addresses the many facets of executive difficulties, and as the name suggests, covers academic, occupational and social deficits. Fifty percent of medication-based treatments for adults with ADHD are ineffective, so psychosocial treatment—although complicated and difficult to apply—is a promising alternative. Psychosocial treatment facilitates marked improvements in major symptoms of executive dysfunction such as time management, organization and self-esteem.

Individuals suffering from endogenous depression require treatment plans that focus on the internal, cognitive thought processes since internal stressors are the root of somatic symptoms. Individual cognitive therapy (ICT) is therefore a common treatment used to gain insight to the individual's internal conflicts or thoughts that are motivating their distressing symptoms. Once the cause of the symptoms are identified, sessions are used to develop new coping skills, behavior modification, and changes in beliefs.

As preventative measures, pharmaceuticals such as SSRI's and antidepressants may also be utilized to avoid further development or progression to Major Depressive Disorder. There have been few treatments targeted specifically toward Endogenous Depression; therefore, symptoms are often managed similarly to Major Depressive Disorder. One such treatment is electroconvulsive therapy (ECT). ECT is used as a treatment option for endogenous depression in adults, however, practitioners avoid the use of ECT in young adolescents due to rates of injury.

there are no USFDA-approved medications for the treatment of mild cognitive impairment. Moreover, as of January 2018, there is no high-quality evidence that supports the efficacy of any pharmaceutical drugs or dietary supplements for improving cognitive symptoms in individuals with mild cognitive impairment. A moderate amount of high-quality evidence supports the efficacy of regular physical exercise for improving cognitive symptoms in individuals with MCI. The clinical trials that established the efficacy of exercise therapy for MCI involved twice weekly exercise over a period of six months. A small amount of high-quality evidence supports the efficacy of cognitive training for improving some measures of cognitive function in individuals with mild cognitive impairment. Due to the heterogeneity among studies which assessed the effect of cognitive training in individuals with MCI, there are no particular cognitive training interventions that have been found to provide greater symptomatic benefits for MCI relative to other forms of cognitive training.

The American Academy of Neurology's (AAN) clinical practice guideline on mild cognitive impairment from January 2018 stated that clinicians "should" identify modifiable risk factors in individuals with MCI, assess functional impairments, provide treatment for any behavioral or neuropsychiatric symptoms, and monitor the individual's cognitive status over time. It also stated that medications which cause cognitive impairment "should" be discontinued or avoided if possible. Due to the lack of evidence supporting the efficacy of cholinesterase inhibitors in individuals with MCI, the AAN guideline stated that clinicians who choose to prescribe them for the treatment of MCI "must" inform patients about the lack of evidence supporting this therapy. The guideline also indicated that clinicians "should" recommend that individuals with MCI engage in regular physical exercise for cognitive symptomatic benefits; clinicians "may" also recommend cognitive training, which appears to provide some symptomatic benefit in certain cognitive measures.

As MCI may represent a prodromal state to clinical Alzheimer's disease, treatments proposed for Alzheimer's disease, such as antioxidants and cholinesterase inhibitors, could potentially be useful; however, there is no evidence to support the efficacy of cholinesterase inhibitors for the treatment of mild cognitive impairment. Two drugs used to treat Alzheimer's disease have been assessed for their ability to treat MCI or prevent progression to full Alzheimer's disease. Rivastigmine failed to stop or slow progression to Alzheimer's disease or to improve cognitive function for individuals with mild cognitive impairment; donepezil showed only minor, short-term benefits and was associated with significant side effects.

In a two-year randomized trial of 168 people with MCI given either high-dose vitamins or placebo, vitamins cut the rate of brain shrinkage by up to half. The vitamins were the three B vitamins folic acid, vitamin B6, and vitamin B12, which inhibit production of the amino acid homocysteine. High blood levels of homocysteine are associated with increased risk of cognitive decline, dementia, and cardiovascular disease. A single study from 2012 showed a possible connection between macronutrient intake and development of MCI. It is also suggested that a dietary pattern with relatively high caloric intake from carbohydrates and low caloric intake from fat and proteins may increase the risk of MCI or dementia in elderly persons

Experimental non-pharmacological treatments for MCI include transcranial magnetic stimulation and transcranial direct current stimulation; the efficacy of these interventions for the treatment of MCI has not yet been established.

There is no cure for canine cognitive dysfunction, but there are medical aids to help mask the symptoms attributed to the disease as it progresses. Therapies are a major form of symptom masking, such as exercise increase, new toys, and learning new commands have shown increases in memory. Changing the dog's diet is also a helpful tool in improving memory and cell membrane health. Medication is also one of the most effective ways to mask the symptoms of CCD. Anipryl (selegiline) is the only drug that has been approved for use on dogs with canine cognitive dysfunction. Anipryl is a drug that is used to treat humans with Parkinson's disease, and has shown drastic improvement in the quality of life in dogs living with CCD.

Depression is a treatable illness. Treatments for a major depressive episode may be obtained in one or more of the following settings: mental health specialists (i.e. psychologist, psychiatrists, social workers, counselors, etc.), mental health centers or organizations, hospitals, outpatient clinics, social service agencies, private clinics, peer support groups, clergy, and employee assistance programs. The treatment plan could include psychotherapy alone, antidepressant medications alone, or a combination of medication and psychotherapy.

For major depressive episodes of severe intensity (multiple symptoms, minimal mood reactivity, severe functional impairment), combined psychotherapy and antidepressant medications are more effective than psychotherapy alone. Patients with severe symptoms may require outpatient treatment or hospitalization.

Psychotherapy, also known as talk therapy, counseling, or psychosocial therapy, is characterized by a patient talking about their condition and mental health issues with a trained therapist. Different types of psychotherapy can be effective for depression. These include cognitive behavioral therapy, interpersonal therapy, dialectical behavior therapy, acceptance and commitment therapy, and mindfulness techniques.

Medications used to treat depression include selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), norepinephrine-dopamine reuptake inhibitors (NDRIs), tricyclic antidepressants, monoamine oxidase inhibitors (MAOIs), and atypical antidepressants such as mirtazapine, which do not fit neatly into any of the other categories. Different antidepressants work better for different individuals. It is often necessary to try several before finding one that works best for a specific patient. Some people may find it necessary to combine medications, which could mean two antidepressants or an antipsychotic medication in addition to an antidepressant. If a person's close relative has responded well to a certain medication, that treatment will likely work well for him or her.

Sometimes, people stop taking antidepressant medications due to side effects, although side effects often become less severe over time. Suddenly stopping treatment or missing several doses may cause withdrawal-like symptoms. Some studies have shown that antidepressants may increase short-term suicidal thoughts or actions, especially in children, adolescents, and young adults. However, antidepressants are more likely to reduce a person's risk of suicide in the long run.

If left untreated, a typical major depressive episode may last for about six months. About 20% of these episodes can last two years or more. About half of depressive episodes end spontaneously. However, even after the major depressive episode is over, 20% to 30% of patients have residual symptoms, which can be distressing and associated with disability.

Glucocorticoid medications have been known to be associated with significant side effects involving behavior and mood, regardless of previous psychiatric or cognitive condition, since the early 1950s. But cognitive side effects of steroid medications involving memory and attention are not as widely publicized and may be misdiagnosed as separate conditions, such as attention deficit disorder (ADHD or ADD) in children or early Alzheimer's disease in elderly patients.

Treatment may involve investigation, reassurance and explanation, and possibly specialist treatment such as antidepressants or cognitive behavioral therapy.

Hypothesized treatment options include the use of antioxidants, cognitive behavior therapy, erythropoietin and stimulant drugs such as methylphenidate, though as the mechanism of PCCI is not well understood the potential treatment options are equally theoretical.

Modafinil, approved for narcolepsy, has been used off-label in trials with people with symptoms of PCCI. Modafinil is a wakefulness-promoting agent that can improve alertness and concentration, and studies have shown it to be effective at least among women treated for breast cancer.

While estrogen hormone supplementation may reverse the symptoms of PCCI in women treated for breast cancer, this carries health risks, including possibly promoting the proliferation of estrogen-responsive breast cancer cells.