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.

Recent studies indicate that the symptoms of SCT in children form two dimensions: daydreamy-spacey and sluggish-lethargic, and that the former are more distinctive of the disorder from ADHD than the latter. This same pattern was recently found in the first study of adults with SCT by Barkley and also in more recent studies of college students. These studies indicated that SCT is probably not a subtype of ADHD but a distinct disorder from it. Yet it is one that overlaps with ADHD in 30–50% of cases of each disorder, suggesting a pattern of comorbidity between two related disorders rather than subtypes of the same disorder. Nevertheless, SCT is strongly correlated with ADHD inattentive and combined subtypes. According to a Norwegian study, "SCT correlated significantly with inattentiveness, regardless of the subtype of ADHD."

Obsessive–compulsive disorder affects about 2.3% of people at some point in their life. Rates during a given year are about 1.2% and it occurs worldwide. It is unusual for symptoms to begin after the age of thirty five and half of people develop problems before twenty. Males and females are affected about equally.

There appear to be some genetic components with identical twins more often affected than non-identical twins. Further, individuals with OCD are more likely to have first-degree family members exhibiting the same disorders than do matched controls. In cases where OCD develops during childhood, there is a much stronger familial link in the disorder than cases in which OCD develops later in adulthood. In general, genetic factors account for 45–65% of the variability in OCD symptoms in children diagnosed with the disorder. Recent evidence supports the possibility of a heritable predisposition for neurological development favouring OCD.

A mutation has been found in the human serotonin transporter gene, hSERT, in unrelated families with OCD.

The relationship between the short and long allele of the 5-HTTLPR gene has been examined in OCD, and a meta analysis found that the S allele was associated with OCD in females only. A systematic review found that while neither allele was associated with OCD overall, in caucasians the L allele was associated with OCD. Another meta analysis observed an increased risk in those with the homozygous S allele, but found the LS genotype to be inversely associated with OCD.

A genome wide association study found OCD to be linked with SNPs near BTBD3 and two SNPs in DLGAP1 in a trio-based analysis, but no SNP reached significance when analyzed with case-control data.

One meta analysis found a small but significant association between a polymorphism in SLC1A1 and OCD.

The relationship between OCD and COMT has been inconsistent, with one meta analysis reporting a significant association, albeit only in men, and another meta analysis reporting no association.

It has been postulated by evolutionary psychologists that moderate versions of compulsive behavior may have had evolutionary advantages. Examples would be moderate constant checking of hygiene, the hearth or the environment for enemies. Similarly, hoarding may have had evolutionary advantages. In this view OCD may be the extreme statistical "tail" of such behaviors, possibly due to a high amount of predisposing genes.

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.

Environmental factors associated with the development of schizophrenia include the living environment, drug use, and prenatal stressors.

Maternal stress has been associated with an increased risk of schizophrenia, possibly in association with reelin. Maternal Stress has been observed to lead to hypermethylation and therefore under-expression of reelin, which in animal models leads to reduction in GABAergic neurons, a common finding in schizophrenia. Maternal nutritional deficiencies, such as those observed during a famine, as well as maternal obesity have also been identified as possible risk factors for schizophrenia. Both maternal stress and infection have been demonstrated to alter fetal neurodevelopment through pro-inflammatory proteins such as IL-8 and TNF.

Parenting style seems to have no major effect, although people with supportive parents do better than those with critical or hostile parents. Childhood trauma, death of a parent, and being bullied or abused increase the risk of psychosis. Living in an urban environment during childhood or as an adult has consistently been found to increase the risk of schizophrenia by a factor of two, even after taking into account drug use, ethnic group, and size of social group. Other factors that play an important role include social isolation and immigration related to social adversity, racial discrimination, family dysfunction, unemployment, and poor housing conditions.

It has been hypothesized that in some people, development of schizophrenia is related to intestinal tract dysfunction such as seen with non-celiac gluten sensitivity or abnormalities in the intestinal flora. A subgroup of persons with schizophrenia present an immune response to gluten different from that found in people with celiac, with elevated levels of certain serum biomarkers of gluten sensitivity such as anti-gliadin IgG or anti-gliadin IgA antibodies.

Estimates of the heritability of schizophrenia is around 80%, which implies that 80% of the individual differences in risk to schizophrenia is explained by individual differences in genetics. These estimates vary because of the difficulty in separating genetic and environmental influences. The greatest single risk factor for developing schizophrenia is having a first-degree relative with the disease (risk is 6.5%); more than 40% of monozygotic twins of those with schizophrenia are also affected. If one parent is affected the risk is about 13% and if both are affected the risk is nearly 50%.

Many genes are known to be involved in schizophrenia, each of small effect and unknown transmission and expression. The summation of these effect sizes into a polygenic risk score can explain at least 7% of the variability in liability for schizophrenia. Around 5% of cases of schizophrenia are understood to be at least partially attributable to rare copy number variants (CNVs), including 22q11, 1q21 and 16p11. These rare CNVs increase the risk of an individual developing the disorder by as much as 20-fold, and are frequently comorbid with autism and intellectual disabilities. There is a genetic relation between the common variants which cause schizophrenia and bipolar disorder, an inverse genetic correlation with intelligence and no genetic correlation with immune disorders.

Bipolar disorder can cause suicidal ideation that leads to suicidal attempts. Individuals whose bipolar disorder begins with a depressive or mixed affective episode seem to have a poorer prognosis and an increased risk of suicide. One out of two people with bipolar disorder attempt suicide at least once during their lifetime and many attempts are successfully completed. The annual average suicide rate is 0.4 percent, which is 10–20 times that of the general population. The standardized mortality ratio from suicide in bipolar disorder is between 18 and 25. The lifetime risk of suicide has been estimated to be as high as 20 percent in those with bipolar disorder.

The causes of bipolar disorder likely vary between individuals and the exact mechanism underlying the disorder remains unclear. Genetic influences are believed to account for 60–80 percent of the risk of developing the disorder indicating a strong hereditary component. The overall heritability of the bipolar spectrum has been estimated at 0.71. Twin studies have been limited by relatively small sample sizes but have indicated a substantial genetic contribution, as well as environmental influence. For bipolar disorder type I, the rate at which identical twins (same genes) will both have bipolar disorder type I (concordance) is estimated at around 40 percent, compared to about 5 percent in fraternal twins. A combination of bipolar I, II, and cyclothymia similarly produced rates of 42 percent and 11 percent (identical and fraternal twins, respectively), with a relatively lower ratio for bipolar II that likely reflects heterogeneity. There is overlap with major (unipolar) depression and if this is also counted in the co-twin the concordance with bipolar disorder rises to 67 percent in identical twins and 19 percent in fraternal twins. The relatively low concordance between fraternal twins brought up together suggests that shared family environmental effects are limited, although the ability to detect them has been limited by small sample sizes.

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.

Stuttering, also known as stammering, is a speech disorder in which the flow of speech is disrupted by involuntary repetitions and prolongations of sounds, syllables, words or phrases as well as involuntary silent pauses or blocks in which the person who stutters is unable to produce sounds. The term "stuttering" is most commonly associated with involuntary sound repetition, but it also encompasses the abnormal hesitation or pausing before speech, referred to by people who stutter as "blocks", and the prolongation of certain sounds, usually vowels or semivowels. According to Watkins et al., stuttering is a disorder of "selection, initiation, and execution of motor sequences necessary for fluent speech production." For many people who stutter, repetition is the primary problem. The term "stuttering" covers a wide range of severity, encompassing barely perceptible impediments that are largely cosmetic to severe symptoms that effectively prevent oral communication. In the world, approximately four times as many men as women stutter, encompassing 70 million people worldwide, or about 1% of the world's population.

The impact of stuttering on a person's functioning and emotional state can be severe. This may include fears of having to enunciate specific vowels or consonants, fears of being caught stuttering in social situations, self-imposed isolation, anxiety, stress, shame, being a possible target of bullying (especially in children), having to use word substitution and rearrange words in a sentence to hide stuttering, or a feeling of "loss of control" during speech. Stuttering is sometimes popularly seen as a symptom of anxiety, but there is actually no direct correlation in that direction (though as mentioned the inverse can be true, as social anxiety may actually develop in individuals as a result of their stuttering).

Stuttering is generally not a problem with the physical production of speech sounds or putting thoughts into words. Acute nervousness and stress do not cause stuttering, but they can trigger stuttering in people who have the speech disorder, and living with a stigmatized disability can result in anxiety and high allostatic stress load (chronic nervousness and stress) that reduce the amount of acute stress necessary to trigger stuttering in any given person who stutters, exacerbating the problem in the manner of a positive feedback system; the name 'stuttered speech syndrome' has been proposed for this condition. Neither acute nor chronic stress, however, itself creates any predisposition to stuttering.

The disorder is also "variable", which means that in certain situations, such as talking on the telephone or in a large group, the stuttering might be more severe or less, depending on whether or not the stutterer is self-conscious about their stuttering. Stutterers often find that their stuttering fluctuates and that they have "good" days, "bad" days and "stutter-free" days. The times in which their stuttering fluctuates can be random. Although the exact etiology, or cause, of stuttering is unknown, both genetics and neurophysiology are thought to contribute. There are many treatments and speech therapy techniques available that may help decrease speech disfluency in some people who stutter to the point where an untrained ear cannot identify a problem; however, there is essentially no cure for the disorder at present. The severity of the person's stuttering would correspond to the amount of speech therapy needed to decrease disfluency. For severe stuttering, long-term therapy and hard work is required to decrease disfluency.

One of the issues that neurobiologists are more concerned is related with the ability of learning and retaining motor skills controlled by the primary motor cortex. Through literature, they have found that primary motor cortex neurons may control skill acquisition and retention. One of the abilities of the motor cortex that allow this control is plasticity which occurs due to the everyday experience of movement repetition. A common substrate of plasticity are the internal system of connections that are located around these regions, creating motor maps.

Various triggers have been associated with switching from euthymic or depressed states into mania. One common trigger of mania is antidepressant therapy. Studies show that the risk of switching while on an antidepressant is between 6-69% percent. Dopaminergic drugs such as reuptake inhibitors and dopamine agonists may also increase risk of switch. Other medication possibly include glutaminergic agents and drugs that alter the HPA axis. Lifestyle triggers include irregular sleep wake schedules and sleep deprivation, as well as extremely emotional or stressful stimuli.

Various genes that have been implicated in genetic studies of bipolar have been manipulated in preclinical animal models to produce syndromes reflecting different aspects of mania. CLOCK and DBP polymorphisms have been linked to bipolar in population studies, and behavioral changes induced by knockout are reversed by lithium treatment. Metabotropic glutamate receptor 6 has been genetically linked to bipolar, and found to be under-expressed in the cortex. Pituitary adenylate cyclase-activating peptide has been associated with bipolar in gene linkage studies, and knockout in mice produces mania like-behavior. Targets of various treatments such as GSK-3, and ERK1 have also demonstrated mania like behavior in preclinical models.

Mania may be associated with strokes, especially cerebral lesions in the right hemisphere.

Deep brain stimulation of the subthalamic nucleus in Parkinson's Disease has been associated with mania, especially with electrodes placed in the ventromedial STN. A proposed mechanism involves increased excitatory input from the STN to dopaminergic nuclei.

The cause of major depressive disorder is unknown. The biopsychosocial model proposes that biological, psychological, and social factors all play a role in causing depression. The diathesis–stress model specifies that depression results when a preexisting vulnerability, or diathesis, is activated by stressful life events. The preexisting vulnerability can be either genetic, implying an interaction between nature and nurture, or schematic, resulting from views of the world learned in childhood.

Childhood abuse, either physical, sexual or psychological are all risk factors for depression, among other psychiatric issues that co-occur such as anxiety and drug abuse. Childhood trauma also correlates with severity of depression, lack of response to treatment and length of illness. However, some are more susceptible to developing mental illness such as depression after trauma, and various genes have been suggested to control susceptibility.

Mania, also known as manic syndrome, is a state of abnormally elevated arousal, affect, and energy level, or "a state of heightened overall activation with enhanced affective expression together with lability of affect." Although mania is often conceived as a "mirror image" to depression, the heightened mood can be either euphoric or irritable; indeed, as the mania intensifies, irritability can be more pronounced and result in violence, or anxiety.

The symptoms of mania include heightened mood (either euphoric or irritable); flight of ideas and pressure of speech; and increased energy, decreased need for sleep, and hyperactivity. They are most plainly evident in fully developed hypomanic states; in full-blown mania, however, they undergo progressively severe exacerbations and become more and more obscured by other signs and symptoms, such as delusions and fragmentation of behavior.

Mania is a syndrome of multiple causes. Although the vast majority of cases occur in the context of bipolar disorder, it is a key component of other psychiatric disorders (as schizoaffective disorder, bipolar type) and may also occur secondary to various general medical conditions, as multiple sclerosis; certain medications, as prednisone; or certain substances of abuse, as cocaine or anabolic steroids. In current DSM-5 nomenclature, hypomanic episodes are separated from the more severe full manic episodes, which, in turn, are characterized as either mild, moderate, or severe, with specifiers with regard to certain symptomatic features (e.g. catatonia, psychosis). Mania, however, may be divided into three stages: hypomania, or stage I; acute mania, or stage II; and delirious mania, or stage III. This "staging" of a manic episode is, in particular, very useful from a descriptive and differential diagnostic point of view.

Mania varies in intensity, from mild mania (hypomania) to delirious mania, marked by such symptoms as disorientation, florid psychosis, incoherence, and catatonia. Standardized tools such as Altman Self-Rating Mania Scale and Young Mania Rating Scale can be used to measure severity of manic episodes. Because mania and hypomania have also long been associated with creativity and artistic talent, it is not always the case that the clearly manic bipolar person needs or wants medical help; such persons often either retain sufficient self-control to function normally or are unaware that they have "gone manic" severely enough to be committed or to commit themselves. Manic persons often can be mistaken for being under the influence of drugs.

The 5-HTTLPR, or serotonin transporter promoter gene's short allele has been associated with increased risk of depression. However, since the 1990s results have been inconsistent, with three recent reviews finding an effect and two finding none. Other genes that have been linked to a GxE interaction include CRHR1, FKBP5 and BDNF, the first two of which are related to the stress reaction of the HPA axis, and the latter of which is involved in neurogenesis.

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 is one of the several types of X-linked intellectual disability. The cause of M2DS is a duplication of the MECP2 or Methyl CpG binding protein 2 gene located on the X chromosome (Xq28). The MeCP2 protein plays a pivotal role in regulating brain function. Increased levels of MECP2 protein results in abnormal neural function and impaired immune system. Mutations in the MECP2 gene are also commonly associated with Rett syndrome in females. Advances in genetic testing and more widespread use of Array Comparative Genomic Hybridization has led to increased diagnosis of MECP2 duplication syndrome. It is thought to represent ~1% of X-linked male mental disability cases.