Glucocorticoids may be useful for short-term therapy to protect against neurodegeneration caused by the extended stress response that characterizes PTSD, but long-term use may actually promote neurodegeneration.

A number of psychotherapy approaches have been designed with the treatment of trauma in mind—EMDR, progressive counting (PC), somatic experiencing, biofeedback, Internal Family Systems Therapy, and sensorimotor psychotherapy.

There is a large body of empirical support for the use of cognitive behavioral therapy for the treatment of trauma-related symptoms, including posttraumatic stress disorder. Institute of Medicine guidelines identify cognitive behavioral therapies as the most effective treatments for PTSD. Two of these cognitive behavioral therapies, prolonged exposure and cognitive processing therapy, are being disseminated nationally by the Department of Veterans Affairs for the treatment of PTSD. Recent studies show that a combination of treatments involving dialectical behavior therapy (DBT), often used for borderline personality disorder, and exposure therapy is highly effective in treating psychological trauma. If, however, psychological trauma has caused dissociative disorders or complex PTSD, the trauma model approach (also known as phase-oriented treatment of structural dissociation) has been proven to work better than simple cognitive approach. Studies funded by pharmaceuticals have also shown that medications such as the new anti-depressants are effective when used in combination with other psychological approaches.

Trauma therapy allows processing trauma-related memories and allows growth towards more adaptive psychological functioning. It helps to develop positive coping instead of negative coping and allows the individual to integrate upsetting-distressing material (thoughts, feelings and memories) resolve internally. It also aids in growth of personal skills like resilience, ego regulation, empathy...etc.

Process' involved in trauma therapy are:

- Psychoeducation: Information dissemination and educating in vulnerabilities and adoptable coping mechanisms.

- Emotional regulation: Identifying, countering discriminating, grounding thoughts and emotions from internal construction to an external representation.

- Cognitive processing: Transforming negative perceptions and beliefs to positive ones about self, others and environment through cognitive reconsideration or re-framing.

- Trauma processing: Systematic desensitization, response activation and counter-conditioning, titrated extinction of emotional response, deconstructing disparity (emotional vs. reality state), resolution of traumatic material (state in which triggers don't produce the harmful distress and able to express relief.)

- Emotional processing: Reconstructing perceptions, beliefs and erroneous expectations like trauma-related fears are auto-activated and habituated in new life contexts, providing crisis cards with coded emotions and appropriate cognition's. (This stage is only initiated in pre-termination phase from clinical assessment & judgement of the mental health professional.)

- Experiential processing: Visualization of achieved relief state and relaxation methods.

Evidence as of 2017 is insufficient to determine if medical cannabis useful for PTSD. Despite the uncertain evidence, use of cannabis or derived products is widespread among U.S. veterans with PTSD.

The cannabinoid nabilone is sometimes used off-label for nightmares in PTSD. Although some short-term benefit was shown, adverse effects are common and it has not been adequately studied to determine efficacy. Additionally, there are other treatments with stronger efficacy and less risks (e.g., psychotherapy, serotonergic antidepressants, adrenergic inhibitors). The use of medical marijuana for PTSD is controversial, with only a handful of states permitting its use for that purpose.

Early childhood trauma refers to psychological trauma experienced in early childhood, in a critical developmental period in a child’s life spanning from conception to the age of five. Trauma experienced in early childhood can manifest across the lifespan and is believed to be associated with a variety of health problems in later life.

Development of psychological resilience is believed to significantly reduce the effects of a childhood trauma on a child’s development.

"See Adverse Childhood Experiences Study"

Adverse childhood experiences (ACEs) are potentially traumatic events that can have negative, lasting effects on health and well-being. Adverse childhood experiences range from abuse to neglect to living in a household where the mother is treated violently or there is a parent with a mental illness. Kaiser Permanente and the Centers for Disease Control and Prevention's 1998 study on adverse childhood experiences determined that traumatic experiences during childhood are a root cause of many social, emotional, and cognitive impairments that lead to increased risk of unhealthy behaviors, risk of violence or re-victimization, chronic health conditions, low life potential and premature mortality. As the number of adverse experiences increases, the risk of problems from childhood through adulthood also rises. Nearly 30 years of study following the initial study has confirmed this. Many states, health providers, and other groups now routinely screen parents and children for ACEs.

Psychological trauma is a type of damage to the mind that occurs as a result of a severely distressing event. Trauma is often the result of an overwhelming amount of stress that exceeds one's ability to cope, or integrate the emotions involved with that experience. A traumatic event involves one's experience, or repeating events of being overwhelmed that can be precipitated in weeks, years, or even decades as the person struggles to cope with the immediate circumstances, eventually leading to serious, long-term negative consequences.

However, trauma differs between individuals, according to their subjective experiences. People will react to similar events differently. In other words, not all people who experience a potentially traumatic event will actually become psychologically traumatized. However, it is possible to develop posttraumatic stress disorder (PTSD) after being exposed to a potentially traumatic event.

This discrepancy in risk rate can be attributed to protective factors some individuals may have that enable them to cope with trauma; they are related to temperamental and environmental factors. Some examples are mild exposure to stress early in life, resilience characteristics, and active seeking of help.

Herman believes recovery from C-PTSD occurs in three stages:

1. establishing safety,

2. remembrance and mourning for what was lost,

3. reconnecting with community and more broadly, society.

Herman believes recovery can only occur within a healing relationship and only if the survivor is empowered by that relationship. This healing relationship need not be romantic or sexual in the colloquial sense of "relationship", however, and can also include relationships with friends, co-workers, one's relatives or children, and the therapeutic relationship.

Complex trauma means complex reactions and this leads to complex treatments. Hence, treatment for C-PTSD requires a multi-modal approach. It has been suggested that treatment for C-PTSD should differ from treatment for PTSD by focusing on problems that cause more functional impairment than the PTSD symptoms. These problems include emotional dysregulation, dissociation, and interpersonal problems. Six suggested core components of complex trauma treatment include:

1. Safety

2. Self-regulation

3. Self-reflective information processing

4. Traumatic experiences integration

5. Relational engagement

6. Positive affect enhancement

Multiple treatments have been suggested for C-PTSD. Among these treatments are experiential and emotionally focused therapy, internal family systems therapy, sensorimotor psychotherapy, eye movement desensitization and reprocessing therapy (EMDR), dialectical behavior therapy (DBT), cognitive behavioral therapy, psychodynamic therapy, family systems therapy and group therapy.

The utility of PTSD derived psychotherapies for assisting children with C-PTSD is uncertain. This area of diagnosis and treatment calls for caution in use of the category C-PTSD. Ford and van der Kolk have suggested that C-PTSD may not be as useful a category for diagnosis and treatment of children as a proposed category of developmental trauma disorder (DTD). For DTD to be diagnosed it requires a

'history of exposure to early life developmentally adverse interpersonal trauma such as sexual abuse, physical abuse, violence, traumatic losses of other significant disruption or betrayal of the child's relationships with primary caregivers, which has been postulated as an etiological basis for complex traumatic stress disorders. Diagnosis, treatment planning and outcome are always relational.'

Since C-PTSD or DTD in children is often caused by chronic maltreatment, neglect or abuse in a care-giving relationship the first element of the biopsychosocial system to address is that relationship. This invariably involves some sort of child protection agency. This both widens the range of support that can be given to the child but also the complexity of the situation, since the agency's statutory legal obligations may then need to be enforced.

A number of practical, therapeutic and ethical principles for assessment and intervention have been developed and explored in the field:

- Identifying and addressing threats to the child's or family's safety and stability are the first priority.

- A relational bridge must be developed to engage, retain and maximize the benefit for the child and caregiver.

- Diagnosis, treatment planning and outcome monitoring are always relational (and) strengths based.

- All phases of treatment should aim to enhance self-regulation competencies.

- Determining with whom, when and how to address traumatic memories.

- Preventing and managing relational discontinuities and psychosocial crises.

Chronic illness can affect a child’s development at any stage. During infancy and childhood chronic illness can be detrimental to the development of secure attachment, interpersonal trust, self-regulation, and/or peer relation skills. During middle adolescence, chronic illness can prevent a child from being in school on a regular basis. This can affect a child’s academic and social competence. During adolescence, chronic illness can affect the development of autonomy and self-image. It can also interfere with peer & romantic relationships, and the desire for independence can lead to poor treatment compliance.

Cognitive Behavioral Therapy (CBT) is one of the most common techniques used to build resilience in children suffering from chronic illnesses. CBT includes the practice of breathing exercises, relaxation training, imagery, distraction methods, coping models, cognitive coping skills, reinforcement for compliance, behavioral rehearsal, role-play and direct coaching. Another intervention that is gaining popularity is the PASS Theory of Intelligence. The PASS Model combines a multitude of interventions to create a well-rounded program to foster resiliency in not only the children but the families affected as well. The goals of the pass model are to minimize trauma symptoms, develop adaptive coping skills, strengthen resiliency, and connect families to support networks.

As mentioned earlier, anti-anxiety, antidepressants and tranquilizers are treatment medications that do not cure, but help control the symptoms of dissociative disorders. The accepted mode of treatment are atypical neuroleptics such as Abilify, Zyprexa, Seroquel and Geodon. Newer-generation anticonvulsants are also highly effective. Quetiapine is initiated at 25–50 mg PO bid and increased by 50 mg PO bid q3d until symptom resolution is achieved. The higher dose should be administered nightly due to the strong sedation effects of the medicine. Other medications such as SSRIs and SNRIs may reduce the anxiety and apprehension of the dissociation.

Keppra may be effective in treating dissociation. Doses are usually kept much lower than for the treatment of seizure disorders. Lamotrigine started at 25 mg and increased by 25 mg every 2 weeks is another option. The effects of these novel anticonvulsants is thought to be secondary to GABA modulation.

Risk factors: People who experience chronic physical, sexual or emotional childhood abuse are at a greater risk of developing dissociative disorders. Children and adults experiencing other traumatic events (including war, natural disasters, kidnapping, torture and invasive medical procedures) also may develop these conditions.

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.

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.

The word "dysregulation" is a neologism created by combining the prefix "dys-" to "regulation". According to "Webster's Dictionary", dys- has various roots. With Latin and Greek roots, it is akin to Old English "tō-", "te-" "apart" and in Sanskrit "dus-"" bad, difficult."

Since feeding and eating disorders in children can cause dangerous risks to the child, it is important to seek treatment as soon as possible. Cognitive behavioral therapy can be incredibly beneficial to children with feeding or eating disorders. Family therapy is usually encouraged in order to keep all members involved in nourishing the child.

Intellectual disability in children can be caused by genetic or environmental factors. The individual could have a natural brain malformation or pre or postnatal damage done to the brain caused by drowning or a traumatic brain injury, for example. Nearly 30 to 50% of individuals with intellectual disability will never know the cause of their diagnosis even after thorough investigation.

Prenatal causes of intellectual disability include:

- Congenital infections such as cytomegalovirus, toxoplasmosis, herpes, syphilis, rubella and human immunodeficiency virus

- Prolonged maternal fever in the first trimester

- Exposure to anticonvulsants or alcohol

- Untreated maternal phenylketonuria (PKU)

- Complications of prematurity, especially in extremely low-birth-weight infants

- Postnatal exposure to lead

Single-gene disorders that result in intellectual disability include:

- Fragile X syndrome

- Neurofibromatosis

- Tuberous sclerosis

- Noonan's syndrome

- Cornelia de Lange's syndrome

These single-gene disorders are usually associated with atypical physical characteristics.

About 1/4 of individuals with intellectual disability have a detectable chromosomal abnormality. Others may have small amounts of deletion or duplication of chromosomes, which may go unnoticed and therefore, undetermined.

Prevention of PTE involves preventing brain trauma in general; protective measures include bicycle helmets and child safety seats. No specific treatment exists to prevent the development of epilepsy after TBI occurs. In the past, antiepileptic drugs were used with the intent of preventing the development of PTE. However, while antiepileptic drugs can prevent early PTS, clinical studies have failed to show that prophylactic use of antiepileptic drugs prevents the development of PTE. Why antiepileptic drugs in clinical trials have failed to stop PTE from developing is not clear, but several explanations have been offered. The drugs may simply not be capable of preventing epilepsy, or the drug trials may have been set up in a way that did not allow a benefit of the drugs to be found (e.g. drugs may have been given too late or in inadequate doses). Animal studies have similarly failed to show much protective effect of the most commonly used seizure medications in PTE trials, such as phenytoin and carbamazepine. Antiepileptic drugs are recommended to prevent late seizures only for people in whom PTE has already been diagnosed, not as a preventative measure. On the basis of the aforementioned studies, no treatment is widely accepted to prevent the development of epilepsy. However, it has been proposed that a narrow window of about one hour after TBI may exist during which administration of antiepileptics could prevent epileptogenesis (the development of epilepsy).

Corticosteroids have also been investigated for the prevention of PTE, but clinical trials revealed that the drugs did not reduce late PTS and were actually linked to an increase in the number of early PTS.

Shortly after TBI, people are given anticonvulsant medication, because seizures that occur early after trauma can increase brain damage through hypoxia, excessive release of excitatory neurotransmitters, increased metabolic demands, and increased pressure within the intracranial space. Medications used to prevent seizures include valproate, phenytoin, and phenobarbital. It is recommended that treatment with anti-seizure medication be initiated as soon as possible after TBI. Prevention of early seizures differs from that of late seizures, because the aim of the former is to prevent damage caused by the seizures, whereas the aim of the latter is to prevent epileptogenesis. Strong evidence from clinical trials suggests that antiepileptic drugs given within a day of injury prevent seizures within the first week of injury, but not after. For example, a 2003 review of medical literature found phenytoin to be preventative of early, but probably not late PTS. In children, anticonvulsants may be ineffective for both early and late seizures. For unknown reasons, prophylactic use of antiepileptic drugs over a long period is associated with an increased risk for seizures. For these reasons, antiepileptic drugs are widely recommended for a short time after head trauma to prevent immediate and early, but not late, seizures. No treatment is widely accepted to prevent the development of epilepsy. However, medications may be given to repress more seizures if late seizures do occur.

STPD is rarely seen as the primary reason for treatment in a clinical setting, but it often occurs as a comorbid finding with other mental disorders. When patients with STPD are prescribed pharmaceuticals, they are most often prescribed the same drugs used to treat patients suffering from schizophrenia including traditional neuroleptics such as haloperidol and thiothixene. In order to decide which type of medication should be used, Paul Markovitz distinguishes two basic groups of schizotypal patients:

- Schizotypal patients who appear to be almost schizophrenic in their beliefs and behaviors (aberrant perceptions and cognitions) are usually treated with low doses of antipsychotic medications, e.g. thiothixene. However, it must be mentioned that long-term efficacy of neuroleptics is doubtful.

- For schizotypal patients who are more obsessive-compulsive in their beliefs and behaviors, SSRIs like Sertraline appear to be more effective.

Lamotrigine, an anti-convulsant, appears to be helpful in dealing with social isolation.

According to Theodore Millon, the schizotypal is one of the easiest personality disorders to identify but one of the most difficult to treat with psychotherapy. Persons with STPD usually consider themselves to be simply eccentric, productive, or nonconformist. As a rule, they underestimate maladaptiveness of their social isolation and perceptual distortions. It is not so easy to gain rapport with people who suffer from STPD due to the fact that increasing familiarity and intimacy usually increase their level of anxiety and discomfort. In most cases they do not respond to informality and humor.

Group therapy is recommended for persons with STPD only if the group is well structured and supportive. Otherwise, it could lead to loose and tangential ideation. Support is especially important for schizotypal patients with predominant paranoid symptoms, because they will have a lot of difficulties even in highly structured groups.

Obsessive-compulsive disorders are treated with various serotonergic antidepressants including the tricyclic antidepressant clomipramine and various SSRI medications. With existing drug therapy, OCD symptoms can be controlled, but not cured. Several of these compounds (including paroxetine, which has an FDA indication) have been tested successfully in conjunction with OCD hoarding.

Antiepileptic drugs may be given to prevent further seizures; these drugs completely eliminate seizures for about 35% of people with PTE. However, antiepileptics only prevent seizures while they are being taken; they do not reduce the occurrence once the patient stops taking the drugs. Medication may be stopped after seizures have been controlled for two years. PTE is commonly difficult to treat with drug therapy, and antiepileptic drugs may be associated with side effects. The antiepileptics carbamazepine and valproate are the most common drugs used to treat PTE; phenytoin may also be used but may increase risk of cognitive side effects such as impaired thinking. Other drugs commonly used to treat PTE include clonazepam, phenobarbitol, primidone, gabapentin, and ethosuximide. Among antiepileptic drugs tested for seizure prevention after TBI (phenytoin, sodium valproate, carbamazepine, phenobarbital), no evidence from randomized controlled trials has shown superiority of one over another.

People whose PTE does not respond to medication may undergo surgery to remove the epileptogenic focus, the part of the brain that is causing the seizures. However surgery for PTE may be more difficult than it is for epilepsy due to other causes, and is less likely to be helpful in PTE than in other forms of epilepsy. It can be particularly difficult in PTE to localize the epileptic focus, in part because TBI may affect diffuse areas of the brain. Difficulty locating the seizure focus is seen as a deterrent to surgery. However, for people with sclerosis in the mesial temporal lobe (in the inner aspect of the temporal lobe), who comprise about one third of people with intractable PTE, surgery is likely to have good outcome. When there are multiple epileptic foci or the focus cannot be localized, and drug therapy is not effective, vagus nerve stimulation is another option for treating PTE.

People with PTE have follow-up visits, in which health care providers monitor neurological and neuropsychological function and assess the efficacy and side effects of medications. As with sufferers of other types of epilepsy, PTE sufferers are advised to exercise caution when performing activities for which seizures could be particularly risky, such as rock climbing.

There is a general lack of consensus in the diagnosis and treatment of DID and research on treatment effectiveness focuses mainly on clinical approaches described in case studies. General treatment guidelines exist that suggest a phased, eclectic approach with more concrete guidance and agreement on early stages but no systematic, empirically-supported approach exists and later stages of treatment are not well described and have no consensus. Even highly experienced therapists have few patients that achieve a unified identity. Common treatment methods include an eclectic mix of psychotherapy techniques, including cognitive behavioral therapy (CBT), insight-oriented therapies, dialectical behavioral therapy (DBT), hypnotherapy and eye movement desensitization and reprocessing (EMDR). Medications can be used for comorbid disorders or targeted symptom relief. Some behavior therapists initially use behavioral treatments such as only responding to a single identity, and then use more traditional therapy once a consistent response is established. Brief treatment due to managed care may be difficult, as individuals diagnosed with DID may have unusual difficulties in trusting a therapist and take a prolonged period to form a comfortable therapeutic alliance. Regular contact (weekly or biweekly) is more common, and treatment generally lasts years—not weeks or months. Sleep hygiene has been suggested as a treatment option, but has not been tested. In general there are very few clinical trials on the treatment of DID, none of which were randomized controlled trials.

Therapy for DID is generally phase oriented. Different alters may appear based on their greater ability to deal with specific situational stresses or threats. While some patients may initially present with a large number of alters, this number may reduce during treatment—though it is considered important for the therapist to become familiar with at least the more prominent personality states as the "host" personality may not be the "true" identity of the patient. Specific alters may react negatively to therapy, fearing the therapist's goal is to eliminate the alter (particularly those associated with illegal or violent activities). A more realistic and appropriate goal of treatment is to integrate adaptive responses to abuse, injury or other threats into the overall personality structure. There is debate over issues such as whether exposure therapy (reliving traumatic memories, also known as abreaction), engagement with alters and physical contact during therapy are appropriate and there are clinical opinions both for and against each option with little high-quality evidence for any position.

Brandt et al., noting the lack of empirical studies of treatment effectiveness, conducted a survey of 36 clinicians expert in treating dissociative disorder (DD) who recommended a three-stage treatment. They agreed that skill building in the first stage is important so the patient can learn to handle high risk, potentially dangerous behavior, as well as emotional regulation, interpersonal effectiveness and other practical behaviors. In addition, they recommended "trauma-based cognitive therapy" to reduce cognitive distortions related to trauma; they also recommended that the therapist deal with the dissociated identities early in treatment. In the middle stage, they recommended graded exposure techniques, along with appropriate interventions as needed. The treatment in the last stage was more individualized; few with DD became integrated into one identity.

The International Society for the Study of Trauma and Dissociation has published guidelines to phase-oriented treatment in adults as well as children and adolescents that are widely used in the field of DID treatment. The first phase of therapy focuses on symptoms and relieving the distressing aspects of the condition, ensuring the safety of the individual, improving the patient's capacity to form and maintain healthy relationships, and improving general daily life functioning. Comorbid disorders such as substance abuse and eating disorders are addressed in this phase of treatment. The second phase focuses on stepwise exposure to traumatic memories and prevention of re-dissociation. The final phase focuses on reconnecting the identities of disparate alters into a single functioning identity with all its memories and experiences intact.

A study was conducted with the goal of developing an "expertise-based prognostic model for the treatment of complex posttraumatic stress disorder (PTSD) and dissociative identity disorder (DID)". Researchers constructed a two-stage survey and factor analyses performed on the survey elements found 51 factors common to complex PTSD and DID. The authors concluded from their findings: "The model is supportive of the current phase-oriented treatment model, emphasizing the strengthening of the therapeutic relationship and the patient's resources in the initial stabilization phase. Further research is needed to test the model's statistical and clinical validity."

Cognitive-behavioral therapy (CBT) is a commonly implemented therapeutic intervention for compulsive hoarding. As part of cognitive behavior therapy, the therapist may help the patient to:

- Discover why he or she is compelled to hoard.

- Learn to organize possessions in order to decide what to discard.

- Develop decision-making skills.

- Declutter the home during in-home visits by a therapist or professional organizer.

- Gain and perform relaxation skills.

- Attend family and/or group therapy.

- Be open to trying psychiatric hospitalization if the hoarding is serious.

- Have periodic visits and consultations to keep a healthy lifestyle.

This modality of treatment usually involves exposure and response prevention to situations that cause anxiety and cognitive restructuring of beliefs related to hoarding. Furthermore, research has also shown that certain CBT protocols have been more effective in treatment than others. CBT programs that specifically address the motivation of the sufferer, organization, acquiring new clutter, and removing current clutter from the home have shown promising results. This type of treatment typically involves in-home work with a therapist combined with between-session homework, the completion of which is associated with better treatment outcomes. Research on Internet-based CBT treatments for the disorder (where participants have access to educational resources, cognitive strategies, and chat groups) has also shown promising results both in terms of short- and long-term recovery.

Other therapeutic approaches that have been found to be helpful are:

1. Motivational interviewing: originated in addiction therapy. This method is significantly helpful when used in hoarding cases in which insight is poor and ambivalence around change is marked.

2. Harm reduction rather than symptom reduction: also borrowed from addiction therapy. The goal is to decrease the harmful implications of the behavior, rather than the hoarding behaviors.

3. Group therapy: reduces social isolation and social anxiety and is cost-effective compared to one-on-one intervention.

4. Eye movement desensitization and reprocessing (EMDR) has been employed, although there is insufficient evidence for EMDR to be considered effective for treating compulsive hoarding (as for treating obsessive-compulsive disorders in general).

Individuals with hoarding behaviors are often described as having low motivation and poor compliance levels, and as being indecisive and procrastinators, which may frequently lead to premature termination (i.e., dropout) or low response to treatment. Therefore, it was suggested that future treatment approaches, and pharmacotherapy in particular, be directed to address the underlying mechanisms of cognitive impairments demonstrated by individuals with hoarding symptoms.

Mental health professionals frequently express frustration regarding hoarding cases, mostly due to premature termination and poor response to treatment. Patients are frequently described as indecisive, procrastinators, recalcitrant, and as having low or no motivation, which can explain why many interventions fail to accomplish significant results. To overcome this obstacle, some clinicians recommend accompanying individual therapy with home visits to help the clinician:

Likewise, certain cases are assisted by professional organizers as well.

It is not known whether PTS increase the likelihood of developing PTE. Early PTS, while not necessarily epileptic in nature, are associated with a higher risk of PTE. However, PTS do not indicate that development of epilepsy is certain to occur, and it is difficult to isolate PTS from severity of injury as a factor in PTE development. About 3% of patients with no early seizures develop late PTE; this number is 25% in those who do have early PTS, and the distinction is greater if other risk factors for developing PTE are excluded. Seizures that occur immediately after an insult are commonly believed not to confer an increased risk of recurring seizures, but evidence from at least one study has suggested that both immediate and early seizures may be risk factors for late seizures. Early seizures may be less of a predictor for PTE in children; while as many as a third of adults with early seizures develop PTE, the portion of children with early PTS who have late seizures is less than one fifth in children and may be as low as one tenth. The incidence of late seizures is about half that in adults with comparable injuries.