SCT is currently not an official diagnosis in DSM-5. But there are rating scales that can be used to screen for SCT symptoms such as the "Concentration Inventory" (for children and adults) or the "Barkley Sluggish Cognitive Tempo Scale-Children and Adolescents (BSCTS-CA)". The "Comprehensive Behaviour Rating Scale for Children" (CBRSC), an older scale, can also be used for SCT as this case study shows.

Although having no diagnosic code either, ICD-10 mentions the SCT group as a reason for why it did not replace the term ""Hyperkinetic Disorder"" with ""ADHD"."

Other mental disorders may produce similar symptoms to SCT (e.g. excessive daydreaming or "staring blankly") and should not be confused with it. Examples might be conditions like depersonalization disorder, dysthymia, thyroid problems, absence seizures, Bipolar II disorder, Kleine–Levin syndrome, forms of autism or schizoid personality disorder. However, the prevalence of SCT in these clinical populations has yet to be empirically and systematically investigated.

Hypoactivity is an inhibition of behavioral or locomotor activity.

Hypoactivity is a characteristic effect of sedative agents and many centrally acting anesthetics. Other drugs such as antipsychotics and mCPP also produce this effect, often as a side effect.

It may be a characteristic symptom of the inattentive type of ADHD (ADHD-PI) and sluggish cognitive tempo.

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.

Formal diagnosis may be performed by a psychologist, psychiatrist, clinical social worker, or other licensed mental health professional. To be diagnosed with OCD, a person must have obsessions, compulsions, or both, according to the Diagnostic and Statistical Manual of Mental Disorders (DSM). The Quick Reference to the 2000 edition of the DSM states that several features characterize clinically significant obsessions and compulsions. Such obsessions, the DSM says, are recurrent and persistent thoughts, impulses or images that are experienced as intrusive and that cause marked anxiety or distress. These thoughts, impulses or images are of a degree or type that lies outside the normal range of worries about conventional problems. A person may attempt to ignore or suppress such obsessions, or to neutralize them with some other thought or action, and will tend to recognize the obsessions as idiosyncratic or irrational.

Compulsions become clinically significant when a person feels driven to perform them in response to an obsession, or according to rules that must be applied rigidly, and when the person consequently feels or causes significant distress. Therefore, while many people who do not suffer from OCD may perform actions often associated with OCD (such as ordering items in a pantry by height), the distinction with clinically significant OCD lies in the fact that the person who suffers from OCD "must" perform these actions, otherwise they will experience significant psychological distress. These behaviors or mental acts are aimed at preventing or reducing distress or preventing some dreaded event or situation; however, these activities are not logically or practically connected to the issue, or they are excessive. In addition, at some point during the course of the disorder, the individual must realize that their obsessions or compulsions are unreasonable or excessive.

Moreover, the obsessions or compulsions must be time-consuming (taking up more than one hour per day) or cause impairment in social, occupational or scholastic functioning. It is helpful to quantify the severity of symptoms and impairment before and during treatment for OCD. In addition to the peron's estimate of the time spent each day harboring obsessive-compulsive thoughts or behaviors, concrete tools can be used to gauge the people’s condition. This may be done with rating scales, such as the Yale–Brown Obsessive Compulsive Scale (Y-BOCS). With measurements like these, psychiatric consultation can be more appropriately determined because it has been standardized.

OCD is sometimes placed in a group of disorders called the obsessive–compulsive spectrum.

OCD is often confused with the separate condition obsessive–compulsive personality disorder (OCPD). OCD is egodystonic, meaning that the disorder is incompatible with the sufferer's self-concept. Because ego dystonic disorders go against a person's self-concept, they tend to cause much distress. OCPD, on the other hand, is egosyntonic—marked by the person's acceptance that the characteristics and behaviours displayed as a result are compatible with their self-image, or are otherwise appropriate, correct or reasonable.

As a result, people with OCD are often aware that their behavior is not rational, are unhappy about their obsessions but nevertheless feel compelled by them. By contrast people with OCPD are not aware of anything abnormal; they will readily explain why their actions are rational, it is usually impossible to convince them otherwise, and they tend to derive pleasure from their obsessions or compulsions.

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.

The doctor will review the person's medical history and perform a complete physical and neurological examination that will include an evaluation of the gait. The doctor may ask the patient to walk in a corridor or climb stairs to observe specific features including:

1. Stance, posture, and base (wide or narrow).

2. Gait initiation (including start hesitation or freezing).

3. Walking speed, stride length, step height, foot clearance.

4. Continuity, symmetry, trunk sway, path deviation, arm swing.

5. Involuntary movements.

6. Ability to turn.

7. Ability to rise from a chair (without using the arms).

8. Chair Testing: Each patient was asked to walk 20–30 feet forward and backward toward the examiner. Patients were then asked to sit in a swivel chair with wheels and to propel the chair forward and backward.

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.

Bipolar disorder is commonly diagnosed during adolescence or early adulthood, but onset can occur throughout the life cycle. The disorder can be difficult to distinguish from unipolar depression and the average delay in diagnosis is 5–10 years after symptoms begin. Diagnosis of bipolar disorder takes several factors into account and considers the self-reported experiences of the symptomatic individual, abnormal behavior reported by family members, friends or co-workers, observable signs of illness as assessed by a clinician, and often a medical work-up to rule-out medical causes. In diagnosis, caregiver-scored rating scales, specifically the mother, has been found to be more accurate than teacher and youth report in predicting identifying youths with bipolar disorder. Assessment is usually done on an outpatient basis; admission to an inpatient facility is considered if there is a risk to oneself or others. The most widely used criteria for diagnosing bipolar disorder are from the American Psychiatric Association's (APA) "Diagnostic and Statistical Manual of Mental Disorders", Fifth Edition (DSM-5) and the World Health Organization's (WHO) "International Statistical Classification of Diseases and Related Health Problems", 10th Edition (ICD-10). The ICD-10 criteria are used more often in clinical settings outside of the U.S. while the DSM criteria are used clinically within the U.S. and are the prevailing criteria used internationally in research studies. The DSM-5, published in 2013, included further and more accurate specifiers compared to its predecessor, the DSM-IV-TR. Semi structured interviews such as the Kiddie Schedule for Affective Disorders and Schizophrenia (KSADS) and the Structured Clinical Interview for DSM-IV (SCID) are used for diagnostic confirmation of bipolar disorder.

Several rating scales for the screening and evaluation of bipolar disorder exist, including the Bipolar spectrum diagnostic scale, Mood Disorder Questionnaire, the General Behavior Inventory and the Hypomania Checklist. The use of evaluation scales cannot substitute a full clinical interview but they serve to systematize the recollection of symptoms. On the other hand, instruments for screening bipolar disorder tend to have lower sensitivity.

Blocq's disease was first considered by Paul Blocq (1860–1896), who described this phenomenon as the loss of memory of specialized movements causing the inability to maintain an upright posture, despite normal function of the legs in the bed. The patient is able to stand up, but as soon as the feet are on the ground, the patient cannot hold himself upright nor walk; however when lying down, the subject conserved the integrity of muscular force and the precision of movements of the lower limbs. The motivation of this study came when a fellow student Georges Marinesco (1864) and Paul published a case of parkinsonian tremor (1893) due to a tumor located in the substantia nigra.

In the third paper published by Paul Blocq, he was trying to determine the neurophysiology behind this disease by relating the cerebral cortex (the decision making) and the spinal cord (the decision executer). His hypothesis was that there would exist an inhibitory influence which exerted and influenced the cortical or spinal centers for standing and walking.

The U.S. Food and Drug Administration (FDA) has not approved any drug for the direct treatment of stuttering. However, the effectiveness of pharmacological agents, such as benzodiazepines, anticonvulsants, antidepressants, antipsychotic and antihypertensive medications, and dopamine antagonists in the treatment of stuttering has been evaluated in studies involving both adults and children.

A comprehensive review of pharmacological treatments of stuttering in 2006 concluded that few of the drug trials were methodologically sound. Of those that were, only one, not unflawed study, showed a reduction in the frequency of stuttering to less than 5% of words spoken. In addition, potentially serious side effects of pharmacological treatments were noted, such as weight gain, sexual dysfunctions and the potential for blood pressure increases. There is one new drug studied especially for stuttering named pagoclone, which was found to be well-tolerated "with only minor side-effects of headache and fatigue reported in a minority of those treated".

There are several other mental disorders with symptoms similar to those seen in bipolar disorder. These disorders include schizophrenia, major depressive disorder, attention deficit hyperactivity disorder (ADHD), and certain personality disorders, such as borderline personality disorder.

Although there are no biological tests that are diagnostic of bipolar disorder, blood tests and/or imaging may be carried out to exclude medical illnesses with clinical presentations similar to that of bipolar disorder. Neurologic diseases such as such as multiple sclerosis, complex partial seizures, strokes, brain tumors, Wilson disease, traumatic brain injury, Huntington's disease, and complex migraines can mimic features of bipolar disorder. An EEG may be used to exclude neurological disorders such as epilepsy, and a CT scan or MRI of the head may be used to exclude brain lesions. Additionally, disorders of the endocrine system such as hypothyroidism, hyperthyroidism, and Cushing's disease are in the differential as is the connective tissue disease systemic lupus erythematosus. Infectious causes of mania which may appear similar to bipolar mania include herpes encephalitis, HIV, influenza, or neurosyphilis. Certain vitamin deficiencies such as pellagra (niacin deficiency), Vitamin B12 deficiency, folate deficiency, and Wernicke Korsakoff syndrome (thiamine deficiency) can also lead to mania.

A review of current and recent medications and drug use is considered to rule out these causes; common medications that can cause manic symptoms include antidepressants, prednisone, Parkinson's disease medications, thyroid hormone, stimulants (including cocaine and methamphetamine), and certain antibiotics.

In the ICD-10 there are several disorders with the manic syndrome: organic manic disorder (), mania without psychotic symptoms (), mania with psychotic symptoms (), other manic episodes (), unspecified manic episode (), manic type of schizoaffective disorder (), bipolar affective disorder, current episode manic without psychotic symptoms (), bipolar affective disorder, current episode manic with psychotic symptoms ().

Among preschoolers, the prognosis for recovery is good. Based on research, about 65% of preschoolers who stutter recover spontaneously in the first two years of stuttering, and about 74% recover by their early teens. In particular, girls seem to recover well. For others, early intervention is effective in helping the child overcome disfluency.

Once stuttering has become established, and the child has developed secondary behaviors, the prognosis is more guarded, and only 18% of children who stutter after five years recover spontaneously. However, with treatment young children may be left with little evidence of stuttering.

With adult people who stutter, there is no known cure, though they may make partial recovery or even complete recovery with intervention. People who stutter often learn to stutter less severely, though others may make no progress with therapy.

Emotional sequelae associated with stuttering primarily relates to state-dependent anxiety related to the speech disorder itself. However, this is typically isolated to social contexts that require speaking, is not a trait anxiety, and this anxiety does not persist if stuttering remits spontaneously. Research attempting to correlate stuttering with generalized or state anxiety, personality profiles, trauma history, or decreased IQ have failed to find adequate empirical support for any of these claims.

A diagnostic assessment may be conducted by a suitably trained general practitioner, or by a psychiatrist or psychologist, who records the person's current circumstances, biographical history, current symptoms, and family history. The broad clinical aim is to formulate the relevant biological, psychological, and social factors that may be impacting on the individual's mood. The assessor may also discuss the person's current ways of regulating mood (healthy or otherwise) such as alcohol and drug use. The assessment also includes a mental state examination, which is an assessment of the person's current mood and thought content, in particular the presence of themes of hopelessness or pessimism, self-harm or suicide, and an absence of positive thoughts or plans. Specialist mental health services are rare in rural areas, and thus diagnosis and management is left largely to primary-care clinicians. This issue is even more marked in developing countries. The mental health examination may include the use of a rating scale such as the Hamilton Rating Scale for Depression or the Beck Depression Inventory or the Suicide Behaviors Questionnaire-Revised. The score on a rating scale alone is insufficient to diagnose depression to the satisfaction of the DSM or ICD, but it provides an indication of the severity of symptoms for a time period, so a person who scores above a given cut-off point can be more thoroughly evaluated for a depressive disorder diagnosis. Several rating scales are used for this purpose.

Primary-care physicians and other non-psychiatrist physicians have more difficulty with underrecognition and undertreatment of depression compared to psychiatric physicians, in part because of the physical symptoms that often accompany depression, in addition to the many potential patient, provider, and system barriers that the authors describe. A review found that non-psychiatrist physicians miss about two-thirds of cases, though this has improved somewhat in more recent studies.

Before diagnosing a major depressive disorder, in general a doctor performs a medical examination and selected investigations to rule out other causes of symptoms. These include blood tests measuring TSH and thyroxine to exclude hypothyroidism; basic electrolytes and serum calcium to rule out a metabolic disturbance; and a full blood count including ESR to rule out a systemic infection or chronic disease. Adverse affective reactions to medications or alcohol misuse are often ruled out, as well. Testosterone levels may be evaluated to diagnose hypogonadism, a cause of depression in men. Vitamin D levels might be evaluated, as low levels of vitamin D have been associated with greater risk for depression.

Subjective cognitive complaints appear in older depressed people, but they can also be indicative of the onset of a dementing disorder, such as Alzheimer's disease. Cognitive testing and brain imaging can help distinguish depression from dementia. A CT scan can exclude brain pathology in those with psychotic, rapid-onset or otherwise unusual symptoms. In general, investigations are not repeated for a subsequent episode unless there is a medical indication.

No biological tests confirm major depression. Biomarkers of depression have been sought to provide an objective method of diagnosis. There are several potential biomarkers, including Brain-Derived Neurotrophic Factor and various functional MRI techniques. One study developed a decision tree model of interpreting a series of fMRI scans taken during various activities. In their subjects, the authors of that study were able to achieve a sensitivity of 80% and a specificity of 87%, corresponding to a negative predictive value of 98% and a positive predictive value of 32% (positive and negative likelihood ratios were 6.15, 0.23, respectively). However, much more research is needed before these tests could be used clinically.

Before beginning treatment for mania, careful differential diagnosis must be performed to rule out secondary causes.

The acute treatment of a manic episode of bipolar disorder involves the utilization of either a mood stabilizer (valproate, lithium, or carbamazepine) or an atypical antipsychotic (olanzapine, quetiapine, risperidone, or aripiprazole). Although hypomanic episodes may respond to a mood stabilizer alone, full-blown episodes are treated with an atypical antipsychotic (often in conjunction with a mood stabilizer, as these tend to produce the most rapid improvement).

When the manic behaviours have gone, long-term treatment then focuses on prophylactic treatment to try to stabilize the patient's mood, typically through a combination of pharmacotherapy and psychotherapy. The likelihood of having a relapse is very high for those who have experienced two or more episodes of mania or depression. While medication for bipolar disorder is important to manage symptoms of mania and depression, studies show relying on medications alone is not the most effective method of treatment. Medication is most effective when used in combination with other bipolar disorder treatments, including psychotherapy, self-help coping strategies, and healthy lifestyle choices.

Lithium is the classic mood stabilizer to prevent further manic and depressive episodes. A systematic review found that long term lithium treatment substantially reduces the risk of bipolar manic relapse, by 42%. Anticonvulsants such as valproate, oxcarbazepine and carbamazepine are also used for prophylaxis. More recent drug solutions include lamotrigine, which is another anticonvulsant. Clonazepam (Klonopin) is also used. Sometimes atypical antipsychotics are used in combination with the previous mentioned medications as well, including olanzapine (Zyprexa) which helps treat hallucinations or delusions, Asenapine (Saphris, Sycrest), aripiprazole (Abilify), risperidone, ziprasidone, and clozapine which is often used for people who do not respond to lithium or anticonvulsants.

Verapamil, a calcium-channel blocker, is useful in the treatment of hypomania and in those cases where lithium and mood stabilizers are contraindicated or ineffective. Verapamil is effective for both short-term and long-term treatment.

Antidepressant monotherapy is not recommended for the treatment of depression in patients with bipolar disorders I or II, and no benefit has been demonstrated by combining antidepressants with mood stabilizers in these patients.

The most widely used criteria for diagnosing depressive conditions are found in the American Psychiatric Association's revised fourth edition of the "Diagnostic and Statistical Manual of Mental Disorders" (DSM-IV-TR), and the World Health Organization's "International Statistical Classification of Diseases and Related Health Problems" (ICD-10), which uses the name "depressive episode" for a single episode and "recurrent depressive disorder" for repeated episodes. The latter system is typically used in European countries, while the former is used in the US and many other non-European nations, and the authors of both have worked towards conforming one with the other.

Both DSM-IV-TR and ICD-10 mark out typical (main) depressive symptoms. ICD-10 defines three typical depressive symptoms (depressed mood, anhedonia, and reduced energy), two of which should be present to determine depressive disorder diagnosis. According to DSM-IV-TR, there are two main depressive symptoms—depressed mood and anhedonia. At least one of these must be present to make a diagnosis of major depressive episode.

Major depressive disorder is classified as a mood disorder in DSM-IV-TR. The diagnosis hinges on the presence of single or recurrent major depressive episodes. Further qualifiers are used to classify both the episode itself and the course of the disorder. The category Depressive Disorder Not Otherwise Specified is diagnosed if the depressive episode's manifestation does not meet the criteria for a major depressive episode. The ICD-10 system does not use the term "major depressive disorder" but lists very similar criteria for the diagnosis of a depressive episode (mild, moderate or severe); the term "recurrent" may be added if there have been multiple episodes without mania.

The syndrome primarily affects young males. Preliminary studies suggest that prevalence may be 1.8 per 10,000 live male births. 50% of those affected do not live beyond 25 years of age, with deaths attributed to the impaired immune function.

M2DS was first described in 1999.

In a Nature article published on November 25, 2015, it was revealed that researchers at the Baylor College of Medicine, led by Dr. Huda Y. Zoghbi, have reversed MECP2 Duplication Syndrome in adult symptomatic mice using antisense therapy. Mice treated with an experimental ASO administered through the central nervous system had a reduction of MECP2 protein to normal levels and symptoms of hypoactivity, anxiety, and abnormal social behavior were resolved. Additionally, the seizure activity of the mice and abnormal EEG discharges were abolished. Initial studies demonstrated that reducing the MECP2 protein levels to the correct amount also normalized the expression of the other genes controlled by the MECP2 protein.