GAD runs in families and is six times more common in the children of someone with the condition.

While anxiety arose as an adaptation, in modern times it is almost always thought of negatively in the context of anxiety disorders. People with these disorders have highly sensitive systems; hence, their systems tend to overreact to seemingly harmless stimuli. Sometimes anxiety disorders occur in those who have had traumatic youths, demonstrating an increased prevalence of anxiety when it appears a child will have a difficult future. In these cases, the disorder arises as a way to predict that the individual’s environment will continue to pose threats.

At a low level, anxiety is not a bad thing. In fact, the hormonal response to anxiety has evolved as a benefit, as it helps humans react to dangers. Researchers in evolutionary medicine believe this adaptation allows humans to realize there is a potential threat and to act accordingly in order to ensure greatest possibility of protection. It has actually been shown that those with low levels of anxiety have a greater risk of death than those with average levels. This is because the absence of fear can lead to injury or death. Additionally, patients with both anxiety and depression were found to have lower morbidity than those with depression alone. The functional significance of the symptoms associated with anxiety includes: greater alertness, quicker preparation for action, and reduced probability of missing threats. In the wild, vulnerable individuals, for example those who are hurt or pregnant, have a lower threshold for anxiety response, making them more alert. This demonstrates a lengthy evolutionary history of the anxiety response.

A study on comorbidity of GAD and other depressive disorders has shown that treatment is not more or less effective when there is some sort of comorbidity of another disorder. The severity of symptoms did not affect the outcome of the treatment process in these cases.

In addition to coexisting with depression, research shows that GAD often coexists with conditions associated with stress, such as irritable bowel syndrome. Patients with GAD can sometimes present with symptoms such as insomnia or headaches as well as pain, cardiac events and interpersonal problems.

Further research suggests that about 20 to 40 percent of individuals with attention deficit hyperactivity disorder have comorbid anxiety disorders, with GAD being the most prevalent.

The World Health Organization's Global Burden of Disease project did not include generalized anxiety disorders. In lieu of global statistics, here are some prevalence rates from around the world:

- Australia: 3 percent of adults

- Canada: Between 3 and 5 percent of adults

- Taiwan: 0.4 percent

- United States: approx. 3.1 percent of people age 18 and over in a given year (9.5 million)

The usual age of onset is variable, from childhood to late adulthood, with the median age of onset being approximately 31 and mean age of onset is 32.7. Most studies find that GAD is associated with an earlier and more gradual onset than the other anxiety disorders. The prevalence of GAD in children is approximately 3%; the prevalence in adolescents is reported as high as 10.8%. When GAD appears in children and adolescents, it typically begins around 8 to 9 years of age.

Populations with a higher rate of diagnosis of GAD are individuals that are traditionally oppressed. This includes individuals with low and middle socio-economic status, separated, divorced, and widowed individuals. Women are twice as likely to develop GAD as men. This is primarily because women are more likely than men to live in poverty, be subject to discrimination, and be sexually and physically abused. African Americans have significantly higher odds of enduring GAD and the disorder often manifests itself in different patterns. Other populations that are more diagnosed with GAD are those who live alone, those with a low level of education, and the unemployed. GAD is also common in the elderly population.

Compared to the general population, patients with internalizing disorders such as depression, generalized anxiety disorder (GAD) and post-traumatic stress disorder (PTSD) have higher mortality rates, but die of the same age-related diseases as the population, such as heart disease, cerebrovascular disease and cancer.

Anxiety disorder, the most common mental illness in the United States, affects 40 million people, ages 10 and older; this accounts for 18% of the U.S. population. Most people suffering from anxiety disorder report some form of racing thoughts symptom

The prevalence of OCD in every culture studied is at least 2% of the population, and the majority of those have obsessions, or racing thoughts. With these reportings, estimates of more than 2 million people in the United States (as of 2000) suffer from racing thoughts.

Various factors have been found to be more associated with a diagnosis of AD than other axis I disorders, including:

- younger age

- more identified psychosocial and environmental problems

- increased suicidal behaviour, more likely to be rated as improved by the time of discharge from mental healthcare

- less frequent previous psychiatric history

- shorter length of treatment

Those exposed to repeated trauma are at greater risk, even if that trauma is in the distant past. Age can be a factor due to young children having fewer coping resources; children are also less likely to assess the consequences of a potential stressor.

A stressor is generally an event of a serious, unusual nature that an individual or group of individuals experience. The stressors that cause adjustment disorders may be grossly traumatic or relatively minor, like loss of a girlfriend/boyfriend, a poor report card, or moving to a new neighborhood. It is thought that the more chronic or recurrent the stressor, the more likely it is to produce a disorder. The objective nature of the stressor is of secondary importance. Stressors' most crucial link to their pathogenic potential is their perception by the patient as stressful. The presence of a causal stressor is essential before a diagnosis of adjustment disorder can be made.

There are certain stressors that are more common in different age groups:

Adulthood:

- Marital conflict

- Financial conflict

- Health issues with Oneself/Partner or Dependent children

- Personal tragedy (Death/personal loss)

- Loss of job or unstable employment conditions (e.g. Corporate takeover/redundancy)

Adolescence and childhood:

- Family conflict/parental separation

- School problems/changing schools

- Sexuality issues

- Death/illness/trauma in the family

In a study conducted from 1990 to 1994 on 89 psychiatric outpatient adolescents, 25% had attempted suicide in which 37.5% had misused alcohol, 87.5% displayed aggressive behaviour, 12.5% had learning difficulties, and 87.5% had anxiety symptoms.

Racing thoughts refers to the rapid thought patterns that often occur in manic, hypomanic, or mixed episodes. While racing thoughts are most commonly described in people with bipolar disorder and sleep apnea, they are also common with anxiety disorders, OCD, and other psychiatric disorders such as attention deficit hyperactivity disorder. Racing thoughts are also associated with sleep deprivation, hyperthyroidism. and the use of amphetamines.

According to the DSM IV-TR, the development of the emotional or behavioral symptoms of this diagnosis have to occur within three months of the onset of the identifiable stressor(s). Some emotional signs of adjustment disorder are:

However, the stress-related disturbance does not only exist as an exacerbation of a pre-existing axis I or axis II disorder and cannot be diagnostic as axis 1 disorder.

Suicidal behavior is prominent among people with AD of all ages, and up to one-fifth of adolescent suicide victims may have an adjustment disorder. Bronish and Hecht (1989) found that 70% of a series of patients with AD attempted suicide immediately before their index admission and they remitted faster than a comparison group with major depression. Asnis et al. (1993) found that AD patients report persistent ideation or suicide attempts less frequently than those diagnosed with major depression. According to a study on 82 AD patients at a clinic, Bolu et al. (2012) found that 22 (26.8%) of these patients were admitted due to suicide attempt, consistent with previous findings. In addition, it was found that 15 of these 22 patients chose suicide methods that involved high chances of being saved. Henriksson et al. (2005) states statistically that the stressors are of one-half related to parental issues and one-third in peer issues.

There is some evidence that a predisposition to night terrors and other parasomnias may be congenital. Individuals frequently report that past family members have had either episodes of sleep terrors or sleepwalking. In some studies, a ten-fold increase in the prevalence of night terrors in first-degree biological relatives has been observed—however, the exact link to inheritance is not known. Familial aggregation has been found suggesting that there is an autosomal mode of inheritance. In addition, some laboratory findings suggest that sleep deprivation and having a fever can increase the likelihood of a night terror episode occurring. Other contributing factors include nocturnal asthma, gastroesophageal reflux, and central nervous system medications. Special consideration must be used when the subject suffers from narcolepsy, as there may be a link. There have been no findings that show a cultural difference between manifestations of night terrors, though it is thought that the significance and cause of night terrors differ within cultures. Evidence suggests that nightmares are more common among women than men.

Also, older children and adults provide highly detailed and descriptive images associated with their sleep terrors compared to younger children, who either cannot recall or only vaguely remember. Sleep terrors in children are also more likely to occur in males than females; in adults, the ratio between sexes is equal. A longitudinal study examined twins, both identical and fraternal, and found that a significantly higher concordance rate of night terror was found in identical twins than in fraternal.

Though the symptoms of night terrors in adolescents and adults are similar, their causes, prognoses, and treatments are qualitatively different. There is some evidence that suggests that night terrors can occur if the sufferer does not eat a proper diet, does not get the appropriate amount or quality of sleep (e.g., because of sleep apnea), or is enduring stressful events. Adults who have experienced sexual abuse are more likely to receive a diagnosis of sleep disorders, including night terrors. Overall, though, adult night terrors are much less common and often respond best to treatments that rectify causes of poor quality or quantity of sleep.

Night terrors typically occur in children between the ages of three and twelve years, with a peak onset in children aged three and a half years old.

An estimated 1–6% of children experience night terrors. Boys and girls of all ethnic backgrounds are affected equally. In children younger than three and a half years old, peak frequency of night terrors is at least one episode per week. Among older children, peak frequency of night terrors is one or two episodes per month. The children will most likely have no recollection of the episode the next day. Pediatric evaluation may be sought to exclude the possibility that the night terrors are caused by seizure disorders or breathing problems. Most children will outgrow sleep terrors.

The progression of SPS depends on whether it is a typical or abnormal form of the condition and the presence of comorbidities. Early recognition and neurological treatment can limit its progression. SPS is generally responsive to treatment, but the condition usually progresses and stabilizes periodically. Even with treatment, quality of life generally declines as stiffness precludes many activities. Some patients require mobility aids due to the risk of falls. About 65 percent of SPS patients are unable to function independently. About ten percent of SPS patients require intensive care at some point; sudden death occurs in about the same number of patients. These deaths are usually caused by metabolic acidosis or an autonomic crisis.

Patients with SPS generally have high amounts of high glutamic acid decarboxylase antibody titers. About 80 percent of SPS patients have GAD antibodies, compared with about one percent of the general population. The overwhelming majority of people who have GAD antibodies do not contract SPS, indicating that systematic synthesis of the antibody is not the sole cause of SPS. GAD, a presynaptic autoantigen, is generally thought to play a key role in the condition, but exact details of the way that autoantibodies affect SPS patients are not known. Most SPS patients with high-titer GAD antibodies also have antibodies that inhibit GABA-receptor-associated protein (GABARAP). Autoantibodies against amphiphysin and gephyrin are also sometimes found in SPS patients. The antibodies appear to interact with antigens in the brain neurons and the spinal cord synapses, causing a functional blockade with gamma-aminobutyric acid. This leads to GABA impairment, which probably causes the stiffness and spasms that characterizes SPS. There are low GABA levels in the motor cortexes of SPS patients.

It is not known why GAD autoimmunity occurs in SPS patients, and whether SPS qualifies as a neuro-autoimmune disorder has been questioned. It is also unknown whether these antibodies are pathogenic. The amount of GAD antibody titers found in SPS patients does not correlate with disease severity, indicating that titre levels do not need to be monitored. It has not been proven that GAD antibodies are sole cause of SPS, and the possibility exists that they are a marker or an epiphenomenon of the condition's cause.

In SPS patients, motor unit neurons fire involuntarily in a way that resembles a normal contraction. Motor unit potentials fire while the patient is at rest, particularly in the stiff muscles. The excessive firing of motor neurons may be caused by malfunctions in spinal and supra-segmental inhibitory networks that utilize GABA. Involuntary actions show up as voluntary on EMG scans; even when the patient tries to relax, there are agonist and antagonist contractions.

In a minority of patients with SPS, breast, ovarian, or lung cancer manifests paraneoplasticly as proximal muscle stiffness. These cancers are associated with the synaptic proteins amphiphysin and gephyrin. Paraneoplastic SPS with amphiphysin antibodies and breast adenocarcinoma tend to occur together. These patients tend not to have GAD antibodies. Passive transfer of the disease by plasma injection has been shown in paraneoplastic SPS but not classical SPS.

There is evidence of genetic risk of SPS. The HLA class II locus makes patients susceptible to the condition. Most SPS patients have the DQB1* 0201 allele. This allele is also associated with type 1 diabetes.

Prognosis is poor, however, current analysis suggests that those associated with thymoma, benign or malignant, show a less favorable prognosis (CASPR2 Ab positive).

Sydenham's chorea is the foremost classic autoimmune basal ganglia disorder. Possible autoimmune mechanism for encephalitis lethargica with Parkinsonian syndrome has been suggested. The evidence for an autoimmune disorder is less clear for paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS). An autoimmune subgroup may exist in Tourette's syndrome, although results remain controversial. Autoimmune movement disorder with basal ganglia encephalitis associated with D2RA have found recently.

It is estimated that between 6-50% of all persons, depending on population, diagnosed with type 2 diabetes might actually have LADA. This number accounts for an estimated 5–10% of the total diabetes population in the U.S. or, as many as 3.5 million persons with LADA. People with LADA typically have a normal BMI or may be underweight due to weight loss prior to diagnosis. Some people with LADA, however, may be overweight to mildly obese.

Contrary to popular belief, some people having LADA do carry a family history of type 2 diabetes.

People with diabetes show an increased rate of urinary tract infection. The reason is bladder dysfunction that is more common in diabetics than in non-diabetics due to diabetic nephropathy. When present, nephropathy can cause a decrease in bladder sensation, which in turn, can cause increased residual urine, a risk factor for urinary tract infections.

Sexual dysfunction in diabetics is often a result of physical factors such as nerve damage and/or poor circulation, and psychological factors such as stress and/or depression caused by the demands of the disease.