PBA is one of the most frequently reported post-stroke behavioral syndromes, with a range of reported prevalence rates from 28% to 52%. The higher prevalence rates tend to be reported in stroke patients who are older and/or who have a history of prior stroke. The relationship between post-stroke depression and PBA is complicated, because the depressive syndrome also occurs with high frequency in stroke survivors. Post-stroke patients with PBA are more depressed than poststroke patients without PBA, and the presence of a depressive syndrome may exacerbate the weeping side of PBA symptoms.

One study of 301 consecutive cases in a clinic setting reported a 5% prevalence. PBA occurred in patients with more severe head injury, and coincided with other neurological features suggestive of pseudobulbar palsy.

The Brain Injury Association of America (BIAA) indicates that approximately 80% of survey respondents experience symptoms of PBA. Results from a recent investigation estimate the prevalence of PBA associated with traumatic brain injury to exceed more than 55% of survivors.

Empirical studies have found that the prognosis for conversion disorder varies widely, with some cases resolving in weeks, and others enduring for years or decades. There is also evidence that there is no cure for Conversion Disorder, and that although patients may go into remission, they can relapse at any point. Furthermore, many patients who are 'cured' continue to have some degree of symptoms indefinitely.

Information on the frequency of conversion disorder in the West is limited, in part due to the complexities of the diagnostic process. In neurology clinics, the reported prevalence of unexplained symptoms among new patients is very high (between 30 and 60%). However, diagnosis of conversion typically requires an additional psychiatric evaluation, and since few patients will see a psychiatrist it is unclear what proportion of the unexplained symptoms are actually due to conversion. Large scale psychiatric registers in the US and Iceland found incidence rates of 22 and 11 newly diagnosed cases per 100,000 person-years, respectively. Some estimates claim that in the general population, between 0.011% and 0.5% of the population have conversion disorder.

Emotional dysregulation (ED) is a term used in the mental health community to refer to an emotional response that is poorly modulated, and does not fall within the conventionally accepted range of emotive response.

Possible manifestations of emotional dysregulation include angry outbursts or behavior outbursts such as destroying or throwing objects, aggression towards self or others, and threats to kill oneself. These variations usually occur in seconds to minutes or hours. Emotional dysregulation can lead to behavioral problems and can interfere with a person's social interactions and relationships at home, in school, or at place of employment.

Emotional dysregulation can be associated with an experience of early psychological trauma, brain injury, or chronic maltreatment (such as child abuse, child neglect, or institutional neglect/abuse), and associated disorders such as reactive attachment disorder. Emotional dysregulation may present in people with psychiatric disorders such as attention deficit hyperactivity disorder, bipolar disorder, borderline personality disorder, narcissistic personality disorder, and complex post-traumatic stress disorder. ED is also found among those with autism spectrum disorders. In such cases as borderline personality disorder, hypersensitivity to emotional stimuli causes a slower return to a normal emotional state. This is manifested biologically by deficits in the frontal cortices of the brain.

Reduced affect display, sometimes referred to as emotional blunting, is a condition of reduced emotional reactivity in an individual. It manifests as a failure to express feelings (affect display) either verbally or non-verbally, especially when talking about issues that would normally be expected to engage the emotions. Expressive gestures are rare and there is little animation in facial expression or vocal inflection. Reduced affect can be symptomatic of autism, schizophrenia, depression, posttraumatic stress disorder, depersonalization disorder, schizoid personality disorder or brain damage. It may also be a side effect of certain medications (e.g., antipsychotics and antidepressants). Individuals with blunted or flat affect show different regional brain activity when compared with typical individuals.

Reduced affect should be distinguished from apathy, which explicitly refers to a lack of emotion, whereas reduced affect is a lack of emotional expression regardless of whether emotion is actually reduced or not.

It is unclear what causes alexithymia, though several theories have been proposed.

Early studies showed evidence that there may be an interhemispheric transfer deficit among people with alexithymia; that is, the emotional information from the right hemisphere of the brain is not being properly transferred to the language regions in the left hemisphere, as can be caused by a decreased corpus callosum, often present in psychiatric patients who have suffered severe childhood abuse. A neuropsychological study in 1997 indicated that alexithymia may be due to a disturbance to the right hemisphere of the brain, which is largely responsible for processing emotions. In addition, another neuropsychological model suggests that alexithymia may be related to a dysfunction of the anterior cingulate cortex. These studies have some shortcomings, however, and the empirical evidence about the neural mechanisms behind alexithymia remains inconclusive.

French psychoanalyst Joyce McDougall objected to the strong focus by clinicians on neurophysiological at the expense of psychological explanations for the genesis and operation of alexithymia, and introduced the alternative term "disaffectation" to stand for psychogenic alexithymia. For McDougall, the disaffected individual had at some point "experienced overwhelming emotion that threatened to attack their sense of integrity and identity", to which they applied psychological defenses to pulverize and eject all emotional representations from consciousness. A similar line of interpretation has been taken up using the methods of phenomenology. McDougall has also noted that all infants are born unable to identify, organize, and speak about their emotional experiences (the word "infans" is from the Latin "not speaking"), and are "by reason of their immaturity inevitably alexithymic". Based on this fact McDougall proposed in 1985 that the alexithymic part of an adult personality could be "an extremely arrested and infantile psychic structure". The first language of an infant is nonverbal facial expressions. The parent's emotional state is important for determining how any child might develop. Neglect or indifference to varying changes in a child's facial expressions without proper feedback can promote an invalidation of the facial expressions manifested by the child. The parent's ability to reflect self-awareness to the child is another important factor. If the adult is incapable of recognizing and distinguishing emotional expressions in the child, it can influence the child's capacity to understand emotional expressions.

Molecular genetic research into alexithymia remains minimal, but promising candidates have been identified from studies examining connections between certain genes and alexithymia among those with psychiatric conditions as well as the general population. A study recruiting a test population of Japanese males found higher scores on the Toronto Alexithymia Scale among those with the 5-HTTLPR homozygous long (L) allele. The 5-HTTLPR region on the serotonin transporter gene influences the transcription of the seretonin transporter that removes serotonin from the synaptic cleft, and is well studied for its association with numerous psychiatric disorders. Another study examining the 5-HT1A receptor, a receptor that binds serotonin, found higher levels of alexithymia among those with the G allele of the Rs6295 polymorphism within the HTR1A gene. Also, a study examining alexithymia in subjects with obsessive-compulsive disorder found higher alexithymia levels associated with the Val/Val allele of the Rs4680 polymorphism in the gene that encodes Catechol-O-methyltransferase (COMT), an enzyme which degrades catecholamine neurotransmitters such as dopamine. These links are tentative, and further research will be needed to clarify how these genes relate to the neurological anomalies found in the brains of people with alexithymia.

Although there is evidence for the role of environmental and neurological factors, the role and influence of genetic factors for developing alexithymia is still unclear. A single large scale Danish study suggested that genetic factors contributed noticeably to the development of alexithymia. However, such twin studies are controversial, as they suffer from the "equal environments assumption" and the "heritability" estimates in no way correspond to actual DNA structures.

Traumatic brain injury is also implicated in the development alexithymia, and those with traumatic brain injury are six times more likely to exhibit alexithymia.

A restricted or constricted affect is a reduction in an individual's expressive range and the intensity of emotional responses.

Alexithymia frequently co-occurs with other disorders. Research indicates that alexithymia overlaps with autism spectrum disorders (ASD). In a 2004 study using the TAS-20, 85% of the adults with ASD fell into the impaired category; almost half of the whole group fell into the severely impaired category. Among the adult control, only 17% was impaired; none of them severely. Fitzgerald & Bellgrove pointed out that, "Like alexithymia, Asperger's syndrome is also characterised by core disturbances in speech and language and social relationships". Hill & Berthoz agreed with Fitzgerald & Bellgrove (2006) and in response stated that "there is some form of overlap between alexithymia and ASDs". They also pointed to studies that revealed impaired theory of mind skill in alexithymia, neuroanatomical evidence pointing to a shared etiology and similar social skills deficits. The exact nature of the overlap is uncertain. Alexithymic traits in AS may be linked to clinical depression or anxiety; the mediating factors are unknown and it is possible that alexithymia predisposes to anxiety.

There are many more psychiatric disorders that overlap with alexithymia. One study found that 41% of Vietnam War veterans with post-traumatic stress disorder (PTSD) were alexithymic. Another study found higher levels of alexithymia among Holocaust survivors with PTSD compared to those without. Higher levels of alexithymia among mothers with interpersonal violence-related PTSD were found in one study to have proportionally less caregiving sensitivity. This latter study suggested that when treating adult PTSD patients who are parents, alexithymia should be assessed and addressed also with attention to the parent-child relationship and the child's social-emotional development.

Single study prevalence findings for other disorders include 63% in anorexia nervosa, 56% in bulimia, 45% to 50% in major depressive disorder, 34% in panic disorder, 28% of social phobics, and 50% in substance abusers. Alexithymia is also exhibited by a large proportion of individuals with acquired brain injuries such as stroke or traumatic brain injury.

Alexithymia is correlated with certain personality disorders, substance use disorders, some anxiety disorders, and sexual disorders, as well as certain physical illnesses, such as hypertension, inflammatory bowel disease, and functional dyspepsia. Alexithymia is further linked with disorders such as migraine headaches, lower back pain, irritable bowel syndrome, asthma, nausea, allergies, and fibromyalgia.

An inability to modulate emotions is a possibility in explaining why some people with alexithymia are prone to discharge tension arising from unpleasant emotional states through impulsive acts or compulsive behaviors such as binge eating, substance abuse, perverse sexual behavior, or anorexia nervosa. The failure to regulate emotions cognitively might result in prolonged elevations of the autonomic nervous system (ANS) and neuroendocrine systems which can lead to somatic diseases. People with alexithymia also show a limited ability to experience positive emotions leading Krystal (1988) and Sifneos (1987) to describe many of these individuals as anhedonic.

There are links between child emotional dysregulation and later psychopathology. For instance, ADHD symptoms are associated with problems with emotional regulation, motivation, and arousal. One study found a connection between emotional dysregulation at 5 and 10 months, and parent-reported problems with anger and distress at 18 months. Low levels of emotional regulation behaviors at 5 months were also related to non-compliant behaviors at 30 months. While links have been found between emotional dysregulation and child psychopathology, the mechanisms behind how early emotional dysregulation and later psychopathology are related are not yet clear.

Serotonin and norepinephrine reuptake inhibitor, venlafaxine, were given to case study KS four months after initial stroke that started symptoms of witzelsucht. Changes back to his original behavior were noticeable after daily dose of 37.5 mg of venlafaxine for two weeks. In subsequent two months, inappropriate jokes and hypersexual behavior were rarely noticed. Due to the rareness of this disorder, not much research into potential treatments has been conducted.

Witzelsucht (from the German "witzeln", meaning to joke or wisecrack, and "sucht", meaning addiction or yearning) is a set of rare neurological symptoms characterized by a tendency to make puns, or tell inappropriate jokes or pointless stories in socially inappropriate situations. A less common symptom is hypersexuality, the tendency to make sexual comments at inappropriate times or situations. Patients do not understand that their behavior is abnormal, therefore are nonresponsive to others' reactions. This disorder is most commonly seen in patients with frontal lobe damage, particularly right frontal lobe tumors or trauma. The disorder remains named in accordance with its reviewed definition by German neurologist Hermann Oppenheim; its first description as the less focused "Moria" ("stupidity"), by German neurologist Moritz Jastrowitz, was in 1888.

Due to similarity of symptoms of the disorder to the mannerisms of Batman's arch-rival Joker, it is sometimes known as 'The Joker Syndrome'

Recent population-based studies have estimated the prevalence of NPH to be about 0.5% in those over 65 years old, with an incidence of about 5.5 patients per 100,000 of people per year. This is in accordance with comparable findings stating that although normal pressure hydrocephalus can occur in both men and women of any age, it is found more often in the elderly population, with a peak onset generally in the sixth to seventh decades.

Anosodiaphoria is a condition in which a person who suffers disability due to brain injury seems indifferent to the existence of their handicap. Anosodiaphoria is specifically used in association with indifference to paralysis. It is a somatosensory agnosia, or a sign of neglect syndrome. It might be specifically associated with defective functioning of the frontal lobe of the right hemisphere.

Joseph Babinski first used the term anosodiaphoria in 1914 to describe a disorder of the body schema in which patients verbally acknowledge a clinical problem (such as hemiparesis) but fail to be concerned about it. Anosodiaphoria follows a stage of anosognosia, in which there may be verbal, explicit denial of the illness, and after several days to weeks, develop the lack of emotional response. Indifference is different from denial because it implies a lack of caring on the part of the patient whom otherwise acknowledges his or her deficit.

Indifference to illness may have an adverse impact on a patient's engagement in neurological rehabilitation, cognitive rehabilitation and physical rehabilitation. Patients are not likely to implement rehabilitation for a condition about which they are indifferent. Although anosognosia often resolves in days to weeks after stroke, anosodiaphoria often persists. Therefore, the therapist has to be creative in their rehabilitation approach in order to maintain the interest of the patient.

Traumatic brain injury (TBI, physical trauma to the brain) can cause a variety of complications, health effects that are not TBI themselves but that result from it. The risk of complications increases with the severity of the trauma; however even mild traumatic brain injury can result in disabilities that interfere with social interactions, employment, and everyday living. TBI can cause a variety of problems including physical, cognitive, emotional, and behavioral complications.

Symptoms that may occur after a concussion – a minor form of traumatic brain injury – are referred to as post-concussion syndrome.

Emotional detachment, in psychology, can mean two different things.

Emotional detachment can be a positive behavior which allows a person to react calmly to highly emotional circumstances/ individuals. Emotional detachment in this sense is a decision to avoid engaging emotional connections, rather than an inability or difficulty in doing so, typically for personal, social, or other reasons. In this sense it can allow people to maintain boundaries, psychic integrity and avoid undesired impact by or upon others, related to emotional demands. As such it is a deliberate mental attitude which avoids engaging the emotions of others.

This detachment does not necessarily mean avoiding empathy; rather it allows the person space needed to rationally choose whether or not to be overwhelmed or manipulated by such feelings. Examples where this is used in a positive sense might include emotional boundary management, where a person avoids emotional levels of engagement related to people who are in some way emotionally overly demanding, such as difficult co-workers or relatives, or is adopted to aid the person in helping others such as a person who trains himself to ignore the "pleading" food requests of a dieting spouse, or indifference by parents towards a child's begging.

Emotional detachment can also be used to describe what is often considered "emotional numbing", "emotional blunting", i.e., dissociation, depersonalization or in its chronic form depersonalization disorder. This type of emotional numbing or blunting is a disconnection from emotion, it is frequently used as a coping/ survival skill during traumatic childhood events such as abuse or severe neglect. Over time and with much use, this can become second nature when dealing with day to day stressors.

Emotional detachment often arises from psychological trauma and is a component in many anxiety and stress disorders. The person, while physically present, moves elsewhere in the mind, and in a sense is "not entirely present", making them sometimes appear preoccupied.

Thus, such detachment is often not as outwardly obvious as other psychiatric symptoms; people with this problem often have emotional systems that are in overdrive. They may have a hard time being a loving family member. They may avoid activities, places, and people associated with any traumatic events they have experienced. The dissociation can also lead to lack of attention and, hence, to memory problems and in extreme cases, amnesia.

A fictional description of the experience of emotional detachment experienced with dissociation and depersonalization was given by Virginia Woolf in "Mrs Dalloway". In that novel the multifaceted sufferings of a war veteran, Septimus Warren Smith, with post-traumatic stress disorder (as this condition was later named) including dissociation, are elaborated in detail. One clinician has called some passages from the novel "classic" portrayals of the symptoms.

There may be more than one reason to account for emotional detachment.

It is known that SSRI (selective serotonin reuptake inhibitor) antidepressants, after taken for a while or taken one after another (if the doctor is trying to see what works), can cause what is called "emotional blunting". In this instance, the individual in question is often unable to cry, even if he or she wants to.

In other cases, the person may seem fully present but operate merely intellectually when emotional connection would be appropriate. This may present an extreme difficulty in giving or receiving empathy and can be related to the spectrum of narcissistic personality disorder.

Emotional detachment also allows acts of extreme cruelty, such as torture and abuse, supported by the decision to not connect empathically with the person concerned. Social ostracism, such as shunning and parental alienation, are other examples where decisions to shut out a person creates a psychological trauma for the shunned party.

Considering these different definitions, the decision as to whether emotional detachment in any given set of circumstances is considered to be a positive or negative mental attitude is a subjective one, and therefore a decision on which different people may not agree.

Individual differences in the physiological stress response may also contribute to the development of emotional eating habits. Those whose adrenal glands naturally secrete larger quantities of glucocorticoids in response to a stressor are more inclined toward hyperphagia, which can act as a physiological catalyst for emotional eating. Additionally, those whose bodies require more time to clear the bloodstream of excess glucocorticoids are similarly predisposed. These biological factors can interact with environmental elements to further trigger hyperphagia, namely the type of stressor the individual is subjected to. Frequent intermittent stressors trigger repeated, sporadic releases of glucocorticoids broken up by intervals too short to allow for a complete return to baseline levels, leading to increased appetite. Those whose lifestyles or careers entail frequent intermittent stressors thus have greater biological incentive to develop patterns of emotional eating.

In the United States, approximately 15 to 20 percent of 5 year old children will develop symptoms related to disorder. Prevalence changes significantly with age. To be more specific, about 33 percent of 5 year-olds, 25 percent of 7 year olds, 15 percent of 9 year olds, 8 percent of 11 year olds, 4 percent of 13 year-olds, and 3 percent of 15 to 17 year-olds. Numbers show that diurnal enuresis is much less common. Overall, about 60 percent of those suffering are male. However, this too depends on age. From ages 4 to 6, the number of boys and girls is about equal. However, the ratio changes so that by 11 years of age there are twice as many boys as girls. Incidence varies with social class with more incidences among those with low socioeconomic status. No evidence has been found related to ethnic differences. Approximately 85% of children with enuresis have primary enuresis because they have never maintained consistent bedwetting behaviors for at least 6 months.

Pain, especially headache, is a common complication following a TBI. Being unconscious and lying still for long periods can cause blood clots to form (deep venous thrombosis), which can cause pulmonary embolism. Other serious complications for patients who are unconscious, in a coma, or in a vegetative state include pressure sores, pneumonia or other infections, and progressive multiple organ failure.

The risk of post-traumatic seizures increases with severity of trauma (image at right) and is particularly elevated with certain types of brain trauma such as cerebral contusions or hematomas. As many as 50% of people with penetrating head injuries will develop seizures. People with early seizures, those occurring within a week of injury, have an increased risk of post-traumatic epilepsy (recurrent seizures occurring more than a week after the initial trauma) though seizures can appear a decade or more after the initial injury and the common seizure type may also change over time. Generally, medical professionals use anticonvulsant medications to treat seizures in TBI patients within the first week of injury only and after that only if the seizures persist.

Neurostorms may occur after a severe TBI. The lower the Glasgow Coma Score (GCS), the higher the chance of Neurostorming. Neurostorms occur when the patient's Autonomic Nervous System (ANS), Central Nervous System (CNS), Sympathetic Nervous System (SNS), and ParaSympathetic Nervous System (PSNS) become severely compromised https://www.brainline.org/story/neurostorm-century-part-1-3-medical-terminology . This in turn can create the following potential life-threatening symptoms: increased IntraCranial Pressure (ICP), tachycardia, tremors, seizures, fevers, increased blood pressure, increased Cerebral Spinal Fluid (CSF), and diaphoresis https://www.brainline.org/story/neurostorm-century-part-1-3-medical-terminology. A variety of medication may be used to help decrease or control Neurostorm episodes https://www.brainline.org/story/neurostorm-century-part-3-3-new-way-life.

Parkinson's disease and other motor problems as a result of TBI are rare but can occur. Parkinson's disease, a chronic and progressive disorder, may develop years after TBI as a result of damage to the basal ganglia. Other movement disorders that may develop after TBI include tremor, ataxia (uncoordinated muscle movements), and myoclonus (shock-like contractions of muscles).

Skull fractures can tear the meninges, the membranes that cover the brain, leading to leaks of cerebrospinal fluid (CSF). A tear between the dura and the arachnoid membranes, called a CSF fistula, can cause CSF to leak out of the subarachnoid space into the subdural space; this is called a subdural hygroma. CSF can also leak from the nose and the ear. These tears can also allow bacteria into the cavity, potentially causing infections such as meningitis. Pneumocephalus occurs when air enters the intracranial cavity and becomes trapped in the subarachnoid space. Infections within the intracranial cavity are a dangerous complication of TBI. They may occur outside of the dura mater, below the dura, below the arachnoid (meningitis), or within the brain itself (abscess). Most of these injuries develop within a few weeks of the initial trauma and result from skull fractures or penetrating injuries. Standard treatment involves antibiotics and sometimes surgery to remove the infected tissue.

Injuries to the base of the skull can damage nerves that emerge directly from the brain (cranial nerves). Cranial nerve damage may result in:

- Paralysis of facial muscles

- Damage to the nerves responsible for eye movements, which can cause double vision

- Damage to the nerves that provide sense of smell

- Loss of vision

- Loss of facial sensation

- Swallowing problems

Hydrocephalus, post-traumatic ventricular enlargement, occurs when CSF accumulates in the brain, resulting in dilation of the cerebral ventricles and an increase in ICP. This condition can develop during the acute stage of TBI or may not appear until later. Generally it occurs within the first year of the injury and is characterized by worsening neurological outcome, impaired consciousness, behavioral changes, ataxia (lack of coordination or balance), incontinence, or signs of elevated ICP.

Any damage to the head or brain usually results in some damage to the vascular system, which provides blood to the cells of the brain. The body can repair small blood vessels, but damage to larger ones can result in serious complications. Damage to one of the major arteries leading to the brain can cause a stroke, either through bleeding from the artery or through the formation of a blood clot at the site of injury, blocking blood flow to the brain. Blood clots also can develop in other parts of the head. Other types of vascular complications include vasospasm, in which blood vessels constrict and restrict blood flow, and the formation of aneurysms, in which the side of a blood vessel weakens and balloons out.

Fluid and hormonal imbalances can also complicate treatment. Hormonal problems can result from dysfunction of the pituitary, the thyroid, and other glands throughout the body. Two common hormonal complications of TBI are syndrome of inappropriate secretion of antidiuretic hormone and hypothyroidism.

Another common problem is spasticity. In this situation, certain muscles of the body are tight or hypertonic because they cannot fully relax.

Episodes of giggle incontinence are embarrassing and socially incapacitating, diminishing the quality of life. Those having the condition learn to adapt by avoiding activities that may bring on laughter. Other approaches include limiting fluid intake, trying to remain seated, and concealing leakage by wearing absorbent pads and dark clothing.

Favorable response to treatment with the ADHD drug methylphenidate (Ritalin) has been reported, but this treatment option is not acceptable to all patient families.

Dr. Lane Robson, of The Children’s Clinic in Calgary, Alberta, says "If a child is having a wetting episode once a month, medicating them daily is probably not a good treatment. If it’s a daily issue, you may have to make that decision."

Patients with dementia who are confined to a nursing home and may have undiagnosed NPH can possibly become independent again once treated. So far only one study was able to evaluate the prevalence of NPH, both diagnosed and undiagnosed, among residents of assisted-living facilities, showing a prevalence in 9 to 14% of the residents.

NPH may be relieved by surgically implanting a ventriculoperitoneal shunt to drain excess cerebrospinal fluid to the abdomen where it is absorbed. Once the shunt is in place, the ventricles usually diminish in size in 3 to 4 days, regardless of the duration of the hydrocephalus. Even though the ventricular swelling diminishes, only 21% of patients show a marked improvement in symptoms. The most likely patients to show improvement are those that show only gait disturbance, mild or no incontinence, and mild dementia. A more recent study (2004) found better outcomes, concluding that if patients with idiopathic normal pressure hydrocephalus are correctly identified, shunt insertion yielded beneficial outcomes in 86% of patients, in either gait disturbance (81%), improved continence (70%), or both. They also observed that measurements in the diagnostic clinical triad, the cortical sulci size, and periventricular lucencies were related to outcome. However, other factors such as age of the patient, symptom duration, dilation of ventricles, and the degree of presurgical dementia were unrelated to outcome.

Emotional eating itself may be a precursor to developing eating disorders such as binge eating or bulimia nervosa. The relationship between emotional eating and other disorders is largely due to the fact that that emotional eating and these disorders share key characteristics. More specifically, they are both related to emotion focused coping, maladaptive coping strategies, and a strong aversion to negative feelings and stimuli. It is important to note that the causal direction has not been definitively established, meaning that while emotional eating is considered a precursor to these eating disorders, it may be also be the consequence of these disorders. The latter hypothesis that emotional eating happens in response to another eating disorder is supported by research that has shown emotional eating to be more common among individuals already suffering from bulimia nervosa.

Certain inherited genes appear to contribute to incontinence. In 1995, Danish researchers announced they had found a site on human chromosome 13 that is responsible, at least in part, for nighttime wetting. If both parents were enuretic, 77% of their children are too; if only one parent was enuretic, then 44% of their offspring are also. Experts believe that other, undetermined genes also may be involved in incontinence.