A 1994 review of 150 cases reported in the literature found that 38% had died with a mean age of death of 2 years. 32% were still alive at the time of the report with a mean age of 4.65. No data were available for the remainder. The author described living with DDS as "walking a multidimensional tight rope".

The cause of DDS is most commonly (96% of patients) an abnormality in the WT1 gene (Wilms tumor suppressor gene). These abnormalities include changes in certain exons (9 and 8) and mutations in some alleles of the WT1 gene. Genetically, the syndrome is due to mutations in the Wilms tumor suppressor gene, WT1, which is on chromosome 11 (11p13). These mutations are usually found in exons 8 or 9, but at least one has been reported in exon 4.

Dialysis disequilibrium syndrome, commonly abbreviated DDS, is the occurrence of neurologic signs and symptoms, attributed to cerebral edema, during or following shortly after intermittent hemodialysis.

Classically, DDS arises in individuals starting hemodialysis due to chronic renal failure and is associated, in particular, with "aggressive" (high solute removal) dialysis. However, it may also arise in fast onset, i.e. acute, renal failure in certain conditions.

The cause of DDS is currently not well understood. There are two theories to explain it; the first theory postulates that urea transport from the brain cells is slowed in chronic renal failure, leading to a large urea concentration gradient, which results in reverse osmosis. The second theory postulates that organic compounds are increased in uremia to protect the brain and result in injury by, like in the first theory, reverse osmosis. More recent studies on rats noted that brain concentrations of organic osmolytes were not increased relative to baseline after rapid dialysis. Cerebral edema was thus attributed to osmotic effects related to a high urea gradient between plasma and brain.

Colitis is inflammation of the colon. Acute cases are medical emergencies as the horse rapidly loses fluid, protein, and electrolytes into the gut, leading to severe dehydration which can result in hypovolemic shock and death. Horses generally present with signs of colic before developing profuse, watery, fetid diarrhea.

Both infectious and non-infectious causes for colitis exist. In the adult horse, "Salmonella", "Clostridium difficile", and "Neorickettsia risticii" (the causative agent of Potomac Horse Fever) are common causes of colitis. Antibiotics, which may lead to an altered and unhealthy microbiota, sand, grain overload, and toxins such as arsenic and cantharidin can also lead to colitis. Unfortunately, only 20–30% of acute colitis cases are able to be definitively diagnosed. NSAIDs can cause slower-onset of colitis, usually in the right dorsal colon (see Right dorsal colitis).

Treatment involves administration of large volumes of intravenous fluids, which can become very costly. Antibiotics are often given if deemed appropriate based on the presumed underlying cause and the horse's CBC results. Therapy to help prevent endotoxemia and improve blood protein levels (plasma or synthetic colloid administration) may also be used if budgetary constraints allow. Other therapies include probiotics and anti-inflammatory medication. Horses that are not eating well may also require parenteral nutrition. Horses usually require 3–6 days of treatment before clinical signs improve.

Due to the risk of endotoxemia, laminitis is a potential complication for horses suffering from colitis, and may become the primary cause for euthanasia. Horses are also at increased risk of thrombophlebitis.

The incidence of colic can be reduced by restricted access to simple carbohydrates including sugars from feeds with excessive molasses, providing clean feed and drinking water, preventing the ingestion of dirt or sand by using an elevated feeding surface, a regular feeding schedule, regular deworming, regular dental care, a regular diet that does not change substantially in content or proportion and prevention of heatstroke. Horses that bolt their feed are at risk of colic, and several management techniques may be used to slow down the rate of feed consumption.

Supplementing with previously mentioned form of pysllium fiber may reduce risk of sand colic if in a high-risk area. Most supplement forms are given one week per month and available wherever equine feed is purchased.

Turnout is thought to reduce the likelihood of colic, although this has not been proven. It is recommended that a horse receive ideally 18 hours of grazing time each day, as in the wild. However, many times this is difficult to manage with competition horses and those that are boarded, as well as for animals that are easy keepers with access to lush pasture and hence at risk of laminitis. Turnout on a dry lot with lower-quality fodder may have similar beneficial effects.

The lifetime prevalence of dissociative disorders varies from 10% in the general population to 46% in psychiatric inpatients. Diagnosis can be made with the help of structured interviews such as the Dissociative Disorders Interview Schedule (DDIS) and the Structured Clinical Interview for DSM-IV Dissociative Disorders (SCID-D), or with the Dissociative Experiences Scale (DES) which is a self-assessment questionnaire. Some diagnostic tests have also been adapted and/or developed for use with children and adolescents such as the Children's Version of the Response Evaluation Measure (REM-Y-71), Child Interview for Subjective Dissociative Experiences, Child Dissociative Checklist (CDC), Child Behavior Checklist (CBCL) Dissociation Subscale, and the Trauma Symptom Checklist for Children Dissociation Subscale.

There are problems with classification, diagnosis and therapeutic strategies of dissociative and conversion disorders which can be understood by the historic context of hysteria. Even current systems used to diagnose DD such as the DSM-IV and ICD-10 differ in the way the classification is determined. In most cases mental health professionals are still hesitant to diagnose patients with Dissociative Disorder, because before they are considered to be diagnosed with Dissociative Disorder these patients have more than likely been diagnosed with major depression, anxiety disorder, and most often post-traumatic disorder.

An important concern in the diagnosis of dissociative disorders is the possibility that the patient may be feigning symptoms in order to escape negative consequences. Young criminal offenders report much higher levels of dissociative disorders, such as amnesia. In one study it was found that 1% of young offenders reported complete amnesia for a violent crime, while 19% claimed partial amnesia. There have also been incidences in which people with dissociative identity disorder provide conflicting testimonies in court, depending on the personality that is present.

Dissociative disorders (DD) are widely believed to have roots in traumatic childhood experience (abuse or loss), but symptomology often goes unrecognized or is misdiagnosed in children and adolescents. There are several reasons why recognizing symptoms of dissociation in children is challenging: it may be difficult for children to describe their internal experiences; caregivers may miss signals or attempt to conceal their own abusive or neglectful behaviors; symptoms can be subtle or fleeting; disturbances of memory, mood, or concentration associated with dissociation may be misinterpreted as symptoms of other disorders.

In addition to developing diagnostic tests for children and adolescents (see above), a number of approaches have been developed to improve recognition and understanding of dissociation in children. Recent research has focused on clarifying the neurological basis of symptoms associated with dissociation by studying neurochemical, functional and structural brain abnormalities that can result from childhood trauma. Others in the field have argued that recognizing disorganized attachment (DA) in children can help alert clinicians to the possibility of dissociative disorders.

Clinicians and researchers also stress the importance of using a developmental model to understand both symptoms and the future course of DDs. In other words, symptoms of dissociation may manifest differently at different stages of child and adolescent development and individuals may be more or less susceptible to developing dissociative symptoms at different ages. Further research into the manifestation of dissociative symptoms and vulnerability throughout development is needed. Related to this developmental approach, more research is required to establish whether a young patient’s recovery will remain stable over time.