an enduring pattern of inner experience and behavior that deviates markedly from the expectations of the individual's culture, is pervasive and inflexible, has an onset in adolescence or early adulthood, is stable over time, and leads to distress or impairment
The personality disorders are divided into three clusters:
Cluster A disorders involve odd or eccentric behaviors and include paranoid, schizoid, and schizotypal personality disorders.
Cluster B disorders involve dramatic, emotional, or erratic behaviors and include antisocial, borderline, histrionic, and narcissistic personality disorders.
Cluster C disorders involve anxiety and fearfulness and include avoidant, dependent, and obsessive-compulsive personality disorders.
With one exception, a diagnosis of a personality disorder can be assigned to a person under the age of 18 when symptoms have been present for at least one year. The exception is antisocial personality disorder, which cannot be assigned to people under 18 years of age.
requires a pervasive pattern of preoccupation with orderliness, perfectionism, and mental and interpersonal control that severely limits flexibility, openness, and efficiency as indicated by at least four of eight symptoms:
-is preoccupied with details, rules, and schedules so the major point of an activity is lost
-shows perfectionism that interferes with task completion
-is excessively devoted to work and productivity to the exclusion of leisure activities and friendships
-is overly conscientious, scrupulous, and inflexible about morality, ethics, or values
-is unable to discard worn-out or worthless objects even when they don't have sentimental value
-is reluctant to delegate work to others unless they'll do it their way
-adopts a miserly spending style toward self and others
-shows rigidity and stubbornness.
As noted in the DSM-5, obsessive-compulsive personality disorder and obsessive-compulsive disorder share some characteristics, but only obsessive-compulsive disorder involves true obsessions and compulsions.
(a) a disturbance in attention and awareness that develops over a short period of time (often hours to a few days), represents a change from baseline attention and awareness, and tends to fluctuate in severity over the course of the day plus
(b) at least one additional disturbance in cognition (e.g., a memory or language impairment).
Symptoms must not be better explained by another pre-existing or evolving neurocognitive disorder and must not occur in the context of a severely reduced level of arousal (e.g., a coma).
There must also be evidence that symptoms are the direct physiological consequence of a medical condition, substance intoxication or withdrawal, and/or exposure to a toxin.
Causes of delirium include a high fever, nutritional deficiency, electrolyte disturbance, renal or hepatic failure, head injury, and certain drugs and medications (e.g., alcohol, lithium, sedatives, anticholinergic drugs), and it's most common in hospitalized older adults.
Treatment involves addressing causal and contributing medical problems and reducing disorientation through environmental manipulation
-ex. providing sufficient lighting, reducing noise, and minimizing the number of visitors.
-In addition, haloperidol or other antipsychotic drug may help reduce agitation and psychotic symptoms.
This disorder accounts for about 60 to 80% of all cases of NCD
(a) meet the criteria for mild or major NCD
(b) have an insidious onset and gradual progression of impairment in one or more cognitive domains that does not interfere with daily activities for mild NCD and two or more cognitive domains that interfere with daily activities for major NCD
(c) meet the criteria for the probable or possible form of the disorder
(d) are not better explained by another disorder.
For major NCD, the diagnosis of probable Alzheimer's disease requires evidence of a causative genetic mutation from genetic testing or family history and/or evidence of a decline in memory and learning and at least one other cognitive domain, a steadily progressive and gradual decline in cognition, and no evidence of a mixed etiology.
-When these criteria are not met, the diagnosis of possible Alzheimer's disease is assigned.
For mild NCD, the diagnosis of probable Alzheimer's disease requires evidence of a causative genetic mutation from genetic testing or family history, while the diagnosis of possible Alzheimer's disease is assigned when there's no evidence of a causative genetic mutation but there's evidence of a decline in memory and learning, a steadily progressive and gradual decline in cognition, and no evidence of a mixed etiology.
The diagnosis of Alzheimer's disease can be definitively confirmed only with a brain biopsy or an autopsy of the brain after death. However, a brain biopsy is rarely done because of the discomfort and risks associated with this procedure.
-Therefore, an in vivo clinical diagnosis requires the presence of characteristic symptoms as well as elimination of other explanations for the symptoms. Eliminating alternative explanations involves obtaining information from a variety of sources including a family history, physical and neurological exams, laboratory tests, CT scan or MRI, mental status evaluation, and neuropsychological testing. Note that several techniques are used to identify Alzheimer's disease in research settings (e.g. molecular imaging, cerebrospinal fluid protein tests, and genetic risk profiling) but are not routinely used for clinical diagnosis.
DSM-IV distinguished between early- and late-onset Alzheimer's disease, with the early-onset subtype applying to individuals whose symptoms had an onset at 65 year of age or younger.
The DSM-V does not make this distinction but states that the onset is usually in the eighth and ninth decades and that individuals with an early onset are more likely to survive the full course of the disease ... [while those with a later onset] are more likely to have numerous medical comorbidities that affect the course and management of the illness.
The term "pseudodementia" is sometimes used to describe depression that has prominent cognitive symptoms. Unlike people with Alzheimer's disease, people with pseudodementia usually respond well to treatment, and they have an abrupt onset of symptoms, exaggerate their cognitive problems, have moderate memory loss and symptoms of melancholia and anxiety, and often say "I don't know in response" to assessment questions.
In contrast, those with Alzheimer's disease have an insidious onset of symptoms, minimize or deny their cognitive problems, have severe memory impairment, and symptoms of apathy and avolition, and often respond to assessment questions with wrong answers
Alzheimer's disease has been linked to chromosomal, neurotransmitter, and brain abnormalities.
Several genetic variants have been identified as risk factors, including the ApoE4 variant on chromosome 19. Neurotransmitter abnormalities include reduced acetylcholine (ACh) and excessive glutamate, which are both known to be involved in learning and memory.
The hallmark brain abnormalities of Alzheimer's disease are amyloid plaques and neurofibrillary tangles, which disrupt cell-to-cell communication.
-Both are due to a build-up of proteins that occurs with normal aging but is more pervasive in individuals with Alzheimer's disease.
-Extracellular amyloid plaques consist of clumps of beta-amyloid protein, which is formed from the breakdown of a larger protein known as amyloid precursor protein (APP).
-Intracellular neurofibrillary tangles are created by an abnormal accumulation of tau protein that results in the formation of threads that join to form tangles.
-Amyloid plaques and neurofibrillary tangles are first evident in medial temporal lobe structures (which include the entorhinal cortex, amygdala, and hippocampus) and, as the disease progresses, they appear in the frontal and parietal lobes and eventually throughout the cortex.
There's also evidence that the locus coeruleus (an area in the brain stem) is the first area of the brain to be affected by Alzheimer's disease and shows abnormalities before the appearance of symptoms.
Note that neuronal loss in the locus coeruleus has also been linked to neurocognitive disorder with Lewy bodies and neurocognitive disorder due to Parkinson's disease.
The progression of Alzheimer's disease can be described in terms of three stages:
-The early stage lasts for about two to four years
--involves anterograde amnesia, personality changes and mood disturbances, impaired attention and judgment, and anomia (difficulty recalling names of familiar people and objects).
-the middle stage lasts for two to 10 years.
--symptoms include increasing anterograde and retrograde amnesia, disorientation to time and place, anxiety or depression, delusions, wandering and pacing, compulsive and repetitive behaviors, impaired speech, disruption in sleep patterns, and problems with normal daily activities.
-the late stage usually lasts for one to three years
--involves severely deteriorated intellectual functioning, severe disorientation, apathy, severely impaired speech, agitation and aggression, urinary and fecal incontinence, loss of basic motor skills, abnormal reflexes, and inability to perform basic activities of daily life.
There's no cure for Alzheimer's disease, but there are treatments that can temporarily reduce specific symptoms.
Cholinesterase inhibitors and memantine are used to reduce or stabilize memory loss, confusion, and other cognitive symptoms.
-Cholinesterase inhibitors include donepezil and rivastigmine and delay the breakdown of ACh, while memantine is an NMDA receptor antagonist and regulates glutamate activity.
Treatment often includes cognitive and behavioral interventions to improve cognitive functioning and reduce problematic behaviors and, as appropriate, antidepressants to alleviate depression and irritability, anxiolytics to reduce anxiety and restlessness, and antipsychotics to reduce behaviors that are related to mania or psychosis or pose a danger to self or others.
Support, skills training, and other interventions for caregivers are also important. They not only benefit the caregivers but also reduce the likelihood that caregivers will place the family member with Alzheimer's disease in a nursing home, which is desirable because remaining at home is associated with better patient outcomes
this disorder is due to the build-up in certain areas of the brain of Lewy bodies, which consist of an abnormal protein.
It's diagnosed when the individual meets the criteria for major or minor NCD and has the required number of core and suggestive features for the probable or possible forms of the disorder, and symptoms have an insidious onset and a gradual progression.
The core features are fluctuating cognition with variations in attention and alertness, recurrent visual hallucinations, and symptoms of parkinsonism that develop after the cognitive symptoms.
Suggestive features are symptoms of rapid eye movement sleep behavior disorder and severe neuroleptic sensitivity.
For probable NCD, the person must have at least two core features or one core feature and one suggestive feature; for possible NCD, the person must have one core feature or one or both suggestive features.
Note that one difference between NCD with Lewy bodies and NCD due to Alzheimer's disease is that, in the former, the prominent early cognitive symptoms are deficits in complex attention and visuospatial and executive functions while, in the latter, the prominent early cognitive symptoms are deficits in learning and memory.
Also, the main difference between NCD with Lewy bodies and NCD due to Parkinson's disease is the sequence of the onset of motor and cognitive symptoms: Motor symptoms precede cognitive symptoms in NCD due to Parkinson's disease, while cognitive symptoms precede (or, in some cases, are concurrent with) motor symptoms in NCD with Lewy bodies.
diagnosed when the individual meets the criteria for major or minor NCD; symptoms are consistent with a vascular etiology as suggested by a temporal relationship between the onset of symptoms and a stroke or other cerebrovascular event or by a prominent decline in complex attention and executive functioning; and there's evidence of cerebrovascular disease from the individual's history, a physical exam, or neuroimaging.
Its prognosis and course depend on the cause and may involve an acute onset with partial recovery, a stepwise decline, or a progressive course with fluctuations in symptom severity and plateaus that vary in duration.
Prevention and intervention efforts target risk and causative factors, which include hypertension, heart disease, diabetes mellitus, obesity, high cholesterol, and heavy cigarette smoking.
when the individual's symptoms meet the criteria for major or mild NCD, symptoms have an insidious onset followed (in most cases) by a very rapid progression of impairment, and symptoms include motor features associated with prion disease or there's biomarker evidence of the disease (e.g., characteristic lesions on an MRI).
The most common type is Creutzfeldt-Jakob disease (CJD). It's characterized by a rapid progression of symptoms that often meet the criteria for major NCD in as few as six months.
Symptoms include confusion and disorientation, impaired memory and judgment, and other neurocognitive deficits; ataxia, myoclonus, chorea, and other prominent motor symptoms; and psychiatric symptoms that may include apathy, anxiety, and/or mood swings.
There are several types of CJD:
-Sporadic CJD is most common and has an unknown etiology
-familial CJD is inherited
-acquired CJD can be due to consuming infected meat (variant CJD) or transmission during a blood transfusion or other medical procedure (iatrogenic CJD).
involving a cluster of cognitive, behavioral, and physiological symptoms indicating that the individual continues using the substance despite significant substance-related problems.
Symptoms represent four categories and for the diagnosis, the person must have two or more symptoms within a 12-month period.
-pharmacological criteria (tolerance and withdrawal)
Substance use disorder can be diagnosed for all classes of substances except caffeine and are further described with specifiers to indicate the severity of the disorder (which is determined by the number of symptoms) and if the person is in early or sustained remission or in a controlled environment.
Treatment for a substance use disorder ordinarily involves an individual psychosocial intervention plus group, family, or marital therapy; a 12-step program; and/or medication (e.g., disulfiram and naltrexone for alcohol use disorder, methadone and naltrexone for opioid use disorder, and nicotine replacement therapy and the antidepressant bupropion for tobacco use disorder).
Studies comparing the effectiveness of various treatments have often found that combined treatments are most effective.
-ex. research on interventions for tobacco use disorder has found that therapy (especially therapies that include problem-solving skills training and social support) and medication (especially nicotine nasal spray and the nicotine receptor partial agonist varenicline) are each effective when used alone, but that interventions that combine therapy and medication are most effective.
Note that no pharmacological treatment has been approved by the FDA for cocaine (stimulant) use disorder and that treatment ordinarily involves cognitive behavior therapy, recovery-focused behavior therapy, or other psychosocial intervention.
One of the best-known approaches to relapse prevention is Marlatt and Gordon's relapse prevention therapy (RPT), which is a cognitive-behavioral approach. It describes substance addiction as a "learned habit pattern" and views lapses following a period of abstinence as being precipitated by a high-risk situation (e.g., a negative emotional state, interpersonal conflict, social pressure).
-It also proposes that a lapse is most likely to turn into a full-blown relapse when the person has poor coping skills, low self-efficacy, and high expectations about the positive effects of alcohol and responds to the lapse with an "abstinence violation effect" - i.e., with negative emotions, guilt, and a sense of personal failure.
-RPT utilizes cognitive and behavioral strategies that enable clients to recognize and deal more effectively with high-risk situations.
--Strategies include training in coping skills, enhancing self-efficacy, challenging myths about the positive outcomes of substance use, cognitive restructuring to view lapses as mistakes rather than the result of personal failure, and altering lifestyle factors that increase exposure or reduce resistance to high-risk situations.
Finally, Project MATCH, a multisite clinical trial, compared the effectiveness of cognitive behavioral coping skills therapy, motivational enhancement therapy, and twelve-step facilitation for clients who had received a DSM-III-R diagnosis of alcohol dependence or abuse.
-It also evaluated the client-treatment matching hypothesis, which predicts that client outcomes can be improved by matching clients with certain characteristics to treatments most appropriate for those characteristics.
--Clients were randomly assigned to one of the three treatments, and clients in each group were categorized in terms of several characteristics (e.g., alcohol involvement, psychiatric severity, anger, and social support for drinking versus abstinence).
--Results indicated that, at one-year and three-year follow-ups, all three treatments had produced significant reductions in drinking, with twelve-step facilitation having a slight advantage over the other two treatments.
---The results also provided some support for the matching hypothesis. For example, at the three-year follow-up, clients whose social networks were supportive of drinking benefited most from twelve-step facilitation, while clients who were high in anger benefited most from motivational enhancement therapy
Opioid Intoxication: involves significant problematic behavioral or psychological changes (e.g., initial euphoria followed by apathy or dysphoria and impaired judgment) plus pupillary constriction and the development of at least one of three symptoms during or shortly after opioid use:
-drowsiness or coma
-impaired attention or memory.
Opioids include opium, heroin, morphine, and codeine, which are derived from the opium poppy, and synthetic and partly-synthetic drugs, which include methadone, oxycodone, hydrocodone, and fentanyl.
Opioid Withdrawal: This diagnosis requires the development of at least three of nine symptoms following cessation of heavy and prolonged opioid use or administration of an opioid antagonist after opioid use: ex., dysphoric mood, nausea or vomiting, muscle aches, diarrhea, yawning, fever, insomnia.
Sedative, Hypnotic, or Anxiolytic Intoxication: involves maladaptive behavioral and psychological changes (e.g., inappropriate sexual or aggressive behavior, mood lability, impaired judgment) with at least one of six symptoms that develop during or shortly after sedative, hypnotic, or anxiolytic use:
-stupor or coma.
Sedative, Hypnotic, or Anxiolytic Withdrawal: This diagnosis requires the development of at least two of eight symptoms within several hours to a few days after cessation or reduction of sedative, hypnotic, or anxiolytic use:
-nausea or vomiting
-transient hallucinations or illusions
-grand mal seizures.
requires a recurrent pattern of an angry/irritable mood, argumentative/defiant behavior, and/or vindictiveness as evidenced by four or more characteristic symptoms that occur during interactions with at least one person who is not a sibling - ex.
-often loses temper
-is angry and resentful
-often deliberately annoys others
-often blames others for his/her mistakes or misbehavior.
Symptoms have lasted for at least six months and have caused distress for the individual or others in the individual's immediate social context or have a negative impact on the individual's functioning.
In young children, ODD is more common in boys than girls but, in older children and adolescents, it occurs about equally often in boys and girls.
About 30% of children who have a diagnosis of ODD eventually receive a diagnosis of conduct disorder, with an early age of onset of symptoms being associated with a higher risk for conduct disorder.
There's no single optimal intervention for individuals with ODD, and the most effective treatments are tailored to the age, symptoms, and needs of the individual child or adolescent.
However, treatment often includes a combination of parent management training, family therapy, cognitive problem-solving skills training, social skills training, and school-based programs
Conduct disorder has been linked to several factors including heredity, neuropsychological factors (e.g., low levels of serotonin), prenatal exposure to opiates or alcohol, and inadequate parenting practices.
Moffitt (1993) distinguishes between two types of antisocial behavior that correspond to DSM-5's childhood-onset and adolescent-onset CD, and she attributes the two types to different factors:
-Her life-course-persistent type involves a pattern of increasingly serious antisocial behaviors that begins in early childhood, continues into adulthood, and is consistent across situations.
--Moffitt describes this type as being due to a combination of neuropsychological deficits that affect the individual's temperament, cognitive abilities, and other characteristics and an adverse child-rearing environment.
-Her adolescence-limited type is a temporary and situational type of antisocial behavior that's due to a "maturity gap" between an adolescent's biological and sexual maturity and his/her social maturity. For individuals with this type, antisocial behaviors are a way to attain mature status.
Moffitt's description of the outcomes of life-course persistent and adolescent-limited types of conduct disorder are consistent with the DSM-5's description of the course of the disorder.
According to the DSM-5, for most individuals, conduct disorder remits by adulthood, and this is especially true for those whose symptoms have an onset in adolescence.
-In contrast, individuals whose symptoms begin in childhood have a worse prognosis and "an increased risk of criminal behavior, conduct disorder, and substance-related disorders in adulthood"
Interventions for conduct disorder are most effective when they include a family intervention.
For example, Patterson, Reid, and Dishion (1992) have developed the parent management training Oregon model (PMTO) that teaches parents effective behavior modification techniques and how to monitor their children's behaviors and use effective disciplinary strategies.
An alternative is multisystemic treatment (MST), which views antisocial behavior as being multidetermined; targets the child or adolescent and his/her family, school, and community; and combines cognitive, behavioral, family systems, and case-management techniques.
Note that research investigating the effectiveness of Scared Straight programs as a prevention or intervention for conduct disorder have found that they tend to have harmful effects, with participation in these programs increasing the likelihood that juvenile offenders and at-risk juveniles will engage in criminal behaviors in the future.
-The studies have also found that confrontational "rap sessions" and nonconfrontational (educational) approaches have similar negative effects and that these programs may have even worse outcomes for seriously delinquent juveniles
involves a marked incongruence between one's assigned gender and one's experienced or expressed gender.
For children with this disorder, the diagnosis requires at least six of eight symptoms that last for at least six months and cause significant distress or impaired functioning:
-ex. a strong desire to be the other gender
-a strong preference for wearing clothes of the other gender
-a strong preference for toys and activities typically used or engaged in by the other gender
-a strong preference for playmates of the opposite gender
-a strong desire for primary and/or secondary sex characteristics of one's experienced gender.
Symptoms have a duration of at least six months and cause clinically significant distress or impaired functioning.
-A specifier is used to indicate if the child has a congenital adrenogenital disorder or other disorder of sex development.
For adolescents and adults, the diagnosis requires at least two of six symptoms that last for at least six months and cause significant distress or impaired functioning:
-ex. a strong desire to be rid of one's primary and/or secondary sex characteristics
-a strong desire to be of the opposite gender
-a strong desire to be treated as the opposite gender
-a strong conviction that one has the feelings and reactions that are characteristic of the opposite gender.
Specifiers are used to indicate if the individual has a disorder of sex development or is in post-transition.
The Dutch protocol and the gender-affirmative model are two approaches to the treatment of gender dysphoria (or, more generally, to the care of gender diverse youth).
-The Dutch protocol is based on the assumption that gender dysphoria, or a transgender identity, persists into adolescence in only a small minority of people. Consequently, for children under 12 years of age, it recommends "watchful waiting" accompanied by support for children and their families.
--Then, at the first signs of puberty, social transition and puberty-blocking drugs are started for children who are persistent in their gender dysphoria. This gives children time to further explore their gender identity and decide if they want to start cross-sex hormone therapy when they're 16 years of age and undergo gender-affirming surgeries after they're 18.
The gender-affirmative model has become the most widely accepted approach and is based on the assumption that "a child of any age may be cognizant of their authentic identity and will benefit from a social transition at any stage of development".
-Social transition is followed, as appropriate, by puberty blockers, cross-sex hormones, and surgeries; and, throughout the transition process, gender issues are addressed with youth and their families in a supportive and non-judgmental way.
-This model also assumes that
--(a) gender variations are not disorders; (b) gender presentations are diverse and vary across cultures; (c) gender is not always binary and may be fluid; and (d) if present, a child's psychological problems are often secondary to negative interpersonal and cultural reactions to the child (e.g., transphobia, homophobia, sexism).
Research on the outcomes of gender confirmation surgery (also known as gender-affirming surgery) has generally found that it's associated with a decrease in gender dysphoria, improved self-satisfaction, and a low incidence of regret. There's also evidence that transgender male patients have somewhat more positive outcomes than transgender female patients do.
Factors that have been linked to positive outcomes include careful diagnostic screening of individuals seeking surgery, psychological stability, adequate social support, and a lack of surgical complications
The DSM-5 defines a paraphilia as involving "intense and persistent sexual interest other than sexual interest in genital stimulation or preparatory fondling with phenotypically normal, physically mature, consenting human partners" and a paraphilic disorder as a paraphilia that "is currently causing distress or impairment to the individual or ... has entailed personal harm, or risk of harm, to others".
Treatments for paraphilic disorders combine cognitive-behavior therapy with other interventions including group therapy, marital therapy, and/or pharmacotherapy.
-Cognitive strategies include cognitive restructuring and empathy and skills training.
-Behavioral strategies are based on classical conditioning and include covert sensitization and orgasmic (masturbatory) reconditioning.
--Covert sensitization is a form of aversive counterconditioning that's conducted in imagination and replaces the sexual arousal elicited by the paraphilic object or behavior with fear or other undesirable response.
--Orgasmic reconditioning involves instructing the person to switch while masturbating from fantasizing about the paraphilic object or behavior to fantasizing about a more appropriate object or behavior.
Drugs used to treat severe forms of this disorder include gonadotropin-releasing hormones (e.g., Lupron) and antiandrogens (e.g., Depo-Provera).
-Although these drugs reduce sexual desire, they have serious side effects and a high risk for relapse as soon as they're discontinued. SSRIs may be prescribed for individuals with less serious disorders to reduce the depression or compulsions that trigger paraphilic behavior
1. Frotteuristic Disorder: This disorder involves recurrent and intense sexual arousal for at least six months from touching or rubbing against a nonconsenting adult as manifested in fantasies, urges, and/or behaviors.
-For the diagnosis, the person must have acted on the urges with a nonconsenting person or experienced significant distress or impaired functioning as the result of the fantasies or urges.
2. Transvestic Disorder: involves cross-dressing for the purpose of sexual arousal for at least six months as manifested in fantasies, urges, and/or behaviors that cause significant distress or impaired functioning.
-Most men with this disorder identify themselves as heterosexual but may have had occasional sexual relations with men, especially when cross-dressed.
3. Pedophilic Disorder: This disorder involves recurrent and intense sexual arousal for at least six months related to fantasies, urges, and/or behaviors involving sexual activity with a child or children 13 years of age or younger.
-The person must have acted on these urges or must have experienced significant distress or interpersonal problems because of them and must be 16 years of age or older and at least five years older than the child or children.
4. Fetishistic Disorder: This disorder involves recurrent and intense sexual arousal for at least six months in response to a nonliving object or specific non-genital body part with the arousal causing significant distress or impaired functioning.
This disorder involves a restriction of energy intake that causes a significantly low body weight for the person's age, sex, developmental trajectory, and physical health.
For the diagnosis, the person must have
(a) an intense fear of gaining weight or becoming fat or engage in behavior that interferes with weight gain and
(b) a disturbance in the way they experience their weight or shape, self-evaluations that are unduly influenced by weight and shape, or a lack of awareness of the seriousness of their low weight.
Specifiers are used to indicate type (restricting or binge-eating/purging), course (in partial remission or full remission), and severity, which is determined by the person's current body mass index.
Anorexia nervosa often co-occurs with depression or an anxiety disorder (especially obsessive-compulsive disorder), and there's evidence that anxiety often precedes the onset of anorexia.
Medical complications are usually the direct result of malnutrition and extreme weight loss, affect nearly all of the major organ systems, and can lead to death.
Anorexia nervosa is a life-threatening disease that often involves frequent relapses before a stable pattern of eating and weight maintenance is attained.
-It's also one of the most difficult disorders to treat because people with this disorder often deny they have an eating problem and resist treatment.
The prognosis for anorexia is generally considered to be poorer than the prognosis for bulimia nervosa, but there's some evidence that long-term outcomes for the two disorders may be more similar than previously believed:
-For example, Eddy and colleagues (2017) assessed the long-term outcomes for patients with anorexia or bulimia and found that 31.4% of those with anorexia and 68.2% of those with bulimia had recovered at the 9-year follow-up but that 62.8% of patients with anorexia and 68.2% of patients with bulimia had recovered at the 22-year follow-up.
The initial treatment goals for anorexia are to restore the person to a healthy weight and address physical complications.
-Subsequent goals include
(a) increasing the person's motivation to participate in treatment;
(b) providing the person with education about healthy nutrition;
(c) helping the person identify and change beliefs, attitudes, and emotions that are contributing to the eating disorder;
(d) treating psychological conditions that are contributing to the eating disorder (e.g., low self-esteem, impulse control problems);
(e) enlisting family support and providing family therapy when appropriate; and
(f) helping the person identify strategies for preventing relapse.
Treatments that have some research support include enhanced cognitive-behavior therapy for eating disorders and family-based treatment for anorexia nervosa:
-Enhanced cognitive-behavior therapy for eating disorders (CBT-E) focuses on four core eating disorder maintaining mechanisms: clinical perfectionism, core low self-esteem, intense mood states, and interpersonal difficulties.
-Family-based treatment (FBT) for anorexia is an outpatient intervention for adolescents who are medically stable and involves three phases: full parental control, gradual return of control to the adolescent, and establishing an age-appropriate level of independence for the adolescent and healthy family relationships.
Although SSRIs have not been found effective for weight restoration, they may be helpful for maintaining weight gain after weight restoration
This disorder involves recurrent episodes of binge eating that are accompanied by a sense of a lack of control, inappropriate compensatory behavior to prevent weight gain (e.g., self-induced vomiting, excessive exercise), and self-evaluation that's excessively influenced by body shape and weight.
For the diagnosis, binge eating and compensatory behavior must occur at least once a week for three months or more.
Specifiers are used to indicate course (in partial or full remission) and severity, which is based on average number of episodes of inappropriate compensatory behavior per week.
Like anorexia nervosa, bulimia nervosa frequently co-occurs with depression or anxiety, with anxiety sometimes preceding the eating disorder.
Most people with this disorder are within the normal weight range or overweight, and medical complications are usually the result of compensatory behavior.
-For example, purging can cause dental erosion, caries, and other dental problems; gastroesophageal reflux, and dehydration, which causes an electrolyte imbalance that can result in heart arrhythmias and death.
The treatment of bulimia nervosa consists of nutritional rehabilitation plus cognitive behavior therapy (CBT) or interpersonal therapy (IPT). CBT and IPT are both evidence-based treatments for bulimia, but CBT is generally preferred because IPT takes longer to produce beneficial effects comparable to those produced by CBT.
SSRIs and tricyclic antidepressants are sometimes used in conjunction with therapy and have been found useful not only for alleviating comorbid depression but also for reducing binge eating and purging in patients without depression.
While studies have consistently found CBT plus an antidepressant to be superior to an antidepressant alone, studies comparing CBT alone to CBT plus an antidepressant have produced inconsistent results:
-Some studies indicate that the combined treatment is most effective; others indicate that the combined treatment is no more effective than CBT alone.
-In addition, there's evidence that the effects vary, depending on the outcome measure.
--For example, Hall, Friedman, and Leach (2008) found that, in terms of full remission of binge and purge episodes, the combined treatment was most effective followed by, in order, CBT alone and antidepressant alone.
--In contrast, CBT alone had the lowest rate of early dropout from treatment followed by, in order, the combined treatment and antidepressant alone.
The enhanced version of cognitive behavior therapy (CBT-E) has been found to be the most effective version of CBT for patients with bulimia.
-It's a transdiagnostic intervention for eating disorders that's based on the assumption that these disorders share the same core psychopathology - i.e., excessive value given to physical appearance and weight. CBT-E consists of four stages:
Stage 1 includes engaging the patient in treatment; jointly creating a formulation of the patient's eating problem that identifies the processes that are maintaining the problem; establishing self-monitoring of eating and relevant behaviors, thoughts, feelings, and events; providing education about weight and eating; and establishing a pattern of regular eating.
Stage 2 is a brief transitional stage that involves reviewing the patient's progress, identifying any new problems and barriers to change, and revising the formulation if necessary.
Stage 3 includes addressing the patient's overevaluation of shape and weight and exploring its origins; identifying events that trigger undesirable eating; and addressing clinical perfectionism, low self-esteem, and interpersonal problems.
Stage 4 consists of helping the patient identify ways to maintain progress and reduce the risk for relapse.
Several studies have evaluated the effectiveness of telepsychology for individuals with bulimia. These studies have generally found that telepsychology and comparable face-to-face interventions produce positive results but differ in terms of some outcomes.
-For example, Mitchell and colleagues (2008) compared manual-based CBT that was delivered face-to-face or via telepsychology. They found that the two modes of delivery were equivalent in terms of acceptability to clients and retention of clients in treatment. However, they also found that rates of abstinence from binge eating and purging were slightly (non-significantly) higher for face-to-face CBT and that face-to-face CBT produced significantly greater reductions in eating-disordered cognitions.
Finally, compared to individuals with anorexia, those with bulimia are more distressed by their symptoms and tend to be more motivated to change their eating behaviors. The benefits of motivation - and, more specifically, autonomous motivation - on treatment outcomes for individuals with bulimia and other eating disorders has been confirmed by several studies.
-For example, Sansfacon, Gauvin, Fletcher, and Cottier (2018) compared the effects of autonomous (intrinsic) and controlled (extrinsic) motivation for reducing symptoms in adults who had received a diagnosis of bulimia nervosa, anorexia nervosa, or other specified feeding or eating disorder. They found that higher levels of autonomous motivation (but not controlled motivation) predicted a greater reduction in overall symptoms and a lower risk for dropping out of treatment.
involves attacks of an irrepressible need to sleep that causes sleep or daytime naps at least three times a week for three months or more.
The diagnosis requires episodes of cataplexy (loss of muscle tone), hypocretin deficiency, or a rapid eye movement latency of 15 minutes or less as determined by nocturnal sleep polysomnography.
Many people with narcolepsy have hypnagogic (vivid hallucinations before falling asleep) or hypnopompic hallucinations (vivid hallucinations just after awakening) and/or experience sleep paralysis when falling asleep or awakening.
Cataplexy is often triggered by a strong emotion, so people with this disorder may attempt to control their emotions to prevent sleep episodes.
The treatment of narcolepsy involves a combination of behavioral strategies and medication.
-Behavioral strategies include establishing good sleep habits, taking daytime naps, and staying active.
-Medications are used to improve alertness and reduce cataplexy:
--Medications for alertness include modafinil and its newer form armodafinil, which increase dopamine levels, and amphetamines and other psychostimulants (e.g., methylphenidate), which increase dopamine levels and, to a lesser degree, serotonin and norepinephrine levels.
--The primary medication for cataplexy is an antidepressant (e.g., venlafaxine, fluoxetine, and clomipramine).
--In addition, sodium oxybate is useful for patients who do not respond to other treatments. It's a derivative of a natural chemical in the brain and is taken at bedtime to improve deep sleep at night and reduce cataplexy and daytime sleepiness
The diagnostic criteria for PTSD differ slightly for adults, adolescents, and children over six years of age and children six years of age and younger.
-However, for individuals of all ages, symptoms must have lasted for more than one month, cause significant distress or impaired functioning, and be due to exposure to actual or threatened death, serious injury, or sexual violence.
-In addition, the symptoms for all age groups represent four types:
--intrusion (e.g., recurrent distressing memories of the event)
--persistent avoidance of stimuli associated with the traumatic event
--negative changes in mood or cognition
--alterations in arousal and reactivity.
PTSD has been linked to several brain abnormalities: Neuroimaging studies have linked it to decreased activity in the medial prefrontal cortex and anterior cingulate cortex, reduced volume of and activity in the hippocampus, and increased responsivity of the amygdala to trauma-related stimuli.
-There's also evidence of abnormalities in several neurotransmitters including increased levels and activity of dopamine, norepinephrine, and glutamate and decreased levels and activity of serotonin and GABA (Sherin & Nemeroff, 2011).
In terms of treatment, APA's (2017) Clinical Practice Guideline for the Treatment of Posttraumatic Stress Disorder (PTSD) in Adults provides recommendations for psychological and pharmacological treatments.
-With regard to psychological treatments, it gives a strong recommendation for cognitive-behavior therapy, cognitive processing therapy (which combines challenging negative cognitions with writing and reading a detailed description of the trauma), cognitive therapy, and prolonged exposure and a conditional recommendation for brief eclectic psychotherapy, EMDR, and narrative exposure therapy.
--Note that research on EMDR (eye movement desensitization and reprocessing) suggests that its positive effects may be due to exposure to memories of the event rather than rapid eye movements (Seidler & Wagner, 2006).
Also note that single-session psychological debriefing, which is also referred to as critical incident stress debriefing and group psychological debriefing, has not been found to be effective and may actually worsen symptoms.
Most studies evaluating the use of telepsychology for treating PTSD have found it to be comparable to face-to-face interventions in terms of effectiveness.
-For example, in their systematic review of studies evaluating telepsychology for veterans with PTSD, Turgoose, Ashwick, and Murphy (2018) found that trauma-focused therapies (e.g., exposure therapy, behavioral activation) delivered via telepsychology or in-person were similar in terms of the reduction of PTSD symptoms, attendance and dropout rates, client satisfaction, and therapist fidelity to treatment protocols.
-However, the studies included in their review did not provide entirely consistent results with regard to the therapeutic alliance: While therapists providing telepsychology said they didn't have trouble developing rapport with clients, some reported barriers to developing a therapeutic alliance, such as the inability to detect nonverbal communications.
The APA Clinical Practice Guideline does not address treatments for children and adolescents, but trauma-focused cognitive-behavior therapy is an evidence-based treatment that was initially designed for children and adolescents 3 to 18 years of age who have experienced sexual abuse and has subsequently been used to treat children and adolescents exposed to other types of trauma. It incorporates family therapy, parenting skills training, and conjoint parent-child therapy.
Finally, with regard to pharmacological treatments for adults, the Clinical Practice Guideline gives a conditional recommendation for the SSRIs fluoxetine, paroxetine, and sertraline and the SNRI venlafaxine.
-These drugs are useful for treating the depression that often accompanies PTSD and may alleviate the core symptoms of re-experiencing, avoidance/numbing, and hyperarousal
The DSM-5 distinguishes between factitious disorder imposed on self and factitious disorder imposed on another.
Individuals with factitious disorder imposed on self falsify or induce physical or psychological symptoms that are associated with a deception (e.g., ingestion of a drug to produce abnormal lab results).
-They present themselves to others as being ill or impaired and engage in the deception even when there's no obvious external reward for doing so.
Factitious disorder imposed on another has the same symptoms except that they're induced in another person (often in a child by his/her mother).
Factitious disorder must be distinguished from malingering, which is included in the DSM-5 with Other Conditions That May Be a Focus of Clinical Attention.
-It involves an intentional production of physical or psychological symptoms for the purpose of obtaining a drug, financial compensation, or other external reward.
-According to the DSM-5, "malingering is differentiated from factitious disorder by the intentional reporting of symptoms for personal gain ... [while] the diagnosis of factitious disorder requires the absence of obvious rewards".
-The DSM-5 also states that malingering should be suspected whenever a person seeks a medical evaluation for legal reasons, there's a marked discrepancy between the person's symptoms and objective findings, the person is uncooperative with evaluation or treatment, and/or the person has antisocial personality disorder.
The forced-choice method has been found useful for detecting malingering and involves presenting the person with test items that require him/her to choose the correct answer from two or more alternatives.
-The use of this method is based on the assumption that people who are malingering will answer items incorrectly at a higher rate than would be expected by chance alone.
--For instance, when each item has two alternative answers (e.g., true or false), malingering is suggested when the person answers more than 50% of the items incorrectly.
Feigned memory loss associated with factitious disorder and malingering must be distinguished from genuine memory loss that's due to traumatic brain injury or other condition:
-For people with genuine memory loss, the beginning and end of the amnestic period are gradual and hazy and these individuals often remember fragments of some events that occurred during that period.
--In contrast, for people with feigned memory loss, the onset and termination of the amnestic period are often sudden, and these individuals do not remember any events that occurred during this period.
-Also, in contrast to people with feigned memory loss, those with genuine memory loss often believe that hints or clues will help them recall their lost memories.
-Finally, several tests can be used to help detect malingering. For example, the Test of Memory Malingering (TOMM) was developed specifically to determine if an individual is feigning memory loss.
--It uses a forced-choice format that requires individuals to respond to items by indicating which of two images was presented to them just prior to testing. Individuals who are malingering perform significantly below chance level (below 50% correct), which indicates they deliberately chose wrong answers.
-Malingering is also suggested when individuals exhibit excessive impairment or an unexpected pattern of responding (e.g., a pattern that's atypical for individuals with genuine impairment) on neuropsychological tests.
this disorder involves developmentally inappropriate and excessive fear or anxiety about being separated from attachment figures as indicated by at least three of eight symptoms
- ex. excessive distress when anticipating or experiencing separation from attachment figures
-persistent reluctance to go to school, work, or other place away from home because of fear of separation from attachment figures
-repeated complaints of physical symptoms when separation from a major attachment figure occurs or is anticipated.
For the diagnosis, symptoms must last for at least four weeks in children and adolescents or six months in adults and cause significant distress or impaired functioning.
Separation anxiety disorder often develops after exposure to a stressful event, such as parental divorce or the death of a relative or a pet.
School refusal is often a manifestation of separation anxiety disorder but, alternatively, may be due to social anxiety disorder or other disorder.
-Children with school refusal want to stay with their parents or other caregivers rather than go to school, and they complain of physical symptoms (e.g., headache, stomachache, nausea) and cry, plead, bargain, or exhibit panic symptoms when the time to go to school approaches.
The preferred treatment for separation anxiety disorder is ordinarily cognitive-behavior therapy (CBT) that includes psychoeducation, exposure, relaxation techniques, and cognitive restructuring, and there's evidence that the effectiveness of CBT for children is increased when it's combined with parent training.
When the disorder involves school refusal, getting the child back to school is an initial treatment goal in order to reduce the risk for social isolation, academic failure, and other secondary impairments
involves intense fear of or anxiety about a specific object or situation accompanied by avoiding the object or situation or enduring it with intense distress.
For the diagnosis, fear or anxiety must be out of proportion to the actual danger posed by the object or situation, must be persistent (ordinarily lasting for at least six months), and must cause significant distress or impaired functioning.
A specifier is used to indicate the type of phobia as animal, natural environment, blood-injection-injury, situational, or other.
Specific phobia is about twice as common in girls than boys, although the rates differ somewhat for different phobic stimuli. Its onset is usually in childhood, with the mean age of onset being about 10 years of age.
Mowrer's (1947) two-factor theory is one explanation for the development of specific phobias.
-It attributes phobic reactions to a combination of classical and operant conditioning:
--Classical conditioning occurs when a previously neutral (non-anxiety arousing) object or event becomes a conditioned stimulus and elicits a conditioned response of anxiety after being paired with an unconditioned stimulus that naturally elicits anxiety.
--Operant conditioning then occurs when the person learns that avoiding the conditioned stimulus allows him/her to avoid experiencing anxiety. In other words, the person's avoidance behavior is negatively reinforced. As a result, the conditioned response is not extinguished because the person never has opportunities to experience the conditioned stimulus without the unconditioned stimulus.
Treatment for specific phobia ordinarily involves using exposure and response prevention to extinguish the conditioned anxiety response by exposing clients to feared objects or situations while preventing them from making their usual avoidance responses.
There are two types of exposure with response prevention and both can be conducted in vivo or in imagination:
-Flooding involves immediately exposing a client to the client's most feared object or situation until the client's anxiety subsides (i.e., is extinguished).
-Graded (graduated) exposure involves constructing a list of about 10 situations that cause anxiety, beginning with an object or situation that elicits a low level of anxiety and ending with the object or situation that elicits the highest level of anxiety.
--For example, for a client who has a fear of heights, the first item in the list might be standing on a chair and the last item might be riding in a ski lift.
---For each item, the client confronts the object or situation until the client's anxiety subsides. When graded exposure is conducted in vivo, the therapist or other person may accompany the client for the initial exposure to each item in the list.
Both types of exposure have been found to be effective, but clients are usually more comfortable with graded exposure and, therefore, are less likely to drop out of therapy prematurely.
There's evidence that in vivo exposure is more effective than exposure in imagination, that therapist-led exposure is more effective than self-directed exposure, and that virtual reality exposure may be as effective as in vivo exposure, especially for fear of heights (acrophobia) and fear of flying.
For some phobias, the effectiveness of exposure increases when it's combined with another intervention. For example, a person with the blood-injection-injury subtype typically reacts to a feared stimulus with a brief initial increase in heart rate and blood pressure that's followed by a decrease in heart rate and blood pressure, which causes the person to faint.
-Therefore, exposure for this subtype is most effective when it's combined with applied tension, which involves repeatedly tensing and relaxing the body's large muscle groups to increase blood pressure and prevent fainting.
involves recurrent unexpected panic attacks with at least one attack being followed by one month or more of persistent concern about additional attacks or their consequences and/or a significant undesirable change in behavior related to the attack.
The DSM-5 defines a panic attack as "an abrupt surge of intense fear or intense discomfort that reaches a peak within minutes" and that involves at least four of 13 symptoms (ex. heart palpitations, sweating, nausea or abdominal distress, dizziness, fear of losing control or "going crazy," fear of dying, paresthesia, derealization or depersonalization).
Because symptoms of a panic attack are similar to those associated with hyperthyroidism, cardiac arrhythmia, and several other medical conditions, those conditions must be ruled out before this diagnosis is assigned.
The treatment of panic disorder often involves a comprehensive cognitive-behavioral intervention.
-An example is panic control treatment, which combines interoceptive exposure with relaxation and other techniques for controlling symptoms.
--Interoceptive exposure involves deliberately exposing the person to the physical symptoms associated with panic attacks by, for example, having the person run in place, spin in a circle, or breathe through a straw.
Some antidepressants (e.g., imipramine) and benzodiazepines have been found useful for alleviating panic attacks, but they're associated with a high relapse rate when used alone.
involves excessive anxiety and worry about multiple events or activities that occur on most days for at least six months.
For the diagnosis, the person must find anxiety and worrying difficult to control, and symptoms must cause significant distress or impaired functioning and include at least three of the following (or at least one for children):
-being easily fatigued
In contrast to people with nonpathological anxiety, those with GAD feel unable to control their worrying, worry about a larger number of events, and are more likely to have associated somatic symptoms.
The DSM-5 notes that the content of a person's worries are age-related, with children and adolescents worrying most about performance and competence in sports and school and catastrophic events and older adults worrying most about their health and the well-being of family members.
Risk factors for GAD include a family history of an anxiety disorder; the temperament dimensions of behavioral inhibition, neuroticism, and harm avoidance; and exposure to childhood trauma or chronic stress.
In addition, systematic reviews of neuroimaging studies have found that GAD is associated with abnormalities in the ventrolateral and dorsolateral prefrontal cortex, anterior cingulate cortex, posterior parietal cortex, amygdala, and hippocampus.
-For example, there's evidence that GAD is associated with reduced connectivity between regions of the prefrontal cortex and anterior cingulate cortex and the amygdala, which suggests there is weak top-down control of amygdala reactivity.
The most effective treatment for GAD is cognitive-behavior therapy which may be combined with pharmacotherapy. The first-line drugs for GAD are the SSRIs and SNRIs, while individuals whose symptoms do not respond to antidepressants may benefit from the anxiolytic buspirone (Buspar) or a benzodiazepine.
OCD involves recurrent obsessions and/or compulsions that are time-consuming (consume more than one hour each day) and/or cause significant distress or impaired functioning:
Obsessions are recurrent and persistent thoughts, urges, or images that the person experiences as intrusive and unwanted, that they attempt to ignore or suppress, and that usually cause marked anxiety or distress.
Compulsions are repetitive behaviors or mental acts that the person feels driven to perform either in response to an obsession or according to rigidly applied rules.
The goal of compulsions is to reduce anxiety or distress or prevent an undesirable situation from happening, but they're excessive or not connected in a realistic way to their goal.
Specifiers are used to indicate the person's level of insight into the veracity of his/her beliefs and the presence of tics.
-Males have an earlier age of onset of this disorder than females do and, consequently, have a slightly higher prevalence rate than females in childhood, while females have a slightly higher prevalence rate than males in adulthood.
-In addition, males more likely than females to have a comorbid tic disorder.
OCD has been linked to lower-than-normal levels of serotonin and elevated activity in several areas of the brain including the caudate nucleus, orbitofrontal cortex, cingulate gyrus, and thalamus.
Exposure and response (ritual) prevention is the treatment-of-choice and may be combined with cognitive restructuring and/or an SSRI or the tricyclic clomipramine.
There's some evidence that combining exposure and response prevention with an SSRI or clomipramine is more effective than either treatment used alone
Bipolar disorder has been linked to heredity, neurotransmitter and brain abnormalities, and circadian rhythm irregularities:
In terms of heredity, twin, family, and adoption studies have confirmed that bipolar disorder has a strong genetic component.
--For example, twin studies report concordance rates of .67 to 1.0 for monozygotic twins and about .20 for dizygotic twins.
Neurotransmitters that have been linked to bipolar disorder include norepinephrine, serotonin, dopamine, and glutamate, and structural and functional abnormalities have been found in several areas of the brain including the prefrontal cortex, amygdala, hippocampus, and basal ganglia.
Circadian rhythm irregularities linked to bipolar disorder include abnormalities in the sleep-wake cycle, the secretion of hormones, appetite, and core body temperature
Treatment often includes a combination of psychosocial interventions and pharmacotherapy.
Evidence-based psychosocial interventions include family focused therapy, psychoeducation, interpersonal and social rhythm therapy, and cognitive-behavior therapy.
With regard to pharmacotherapy, lithium is usually most effective for "classic bipolar disorder" which is characterized by separation of manic/hypomanic and depressive episodes by long periods of recovery, a low likelihood of mixed mood states and rapid cycling, and an onset between 15 and 19 years of age.
In contrast, anticonvulsant and second generation antipsychotic drugs are most effective for "atypical bipolar disorder," which is characterized by mixed mood states, rapid cycling, a lack of full recovery between episodes, and an onset between 10 and 15 years of age (Aiken, 2018).
-Note that this distinction between classic and bipolar disorder is not a DSM-5 categorization and that DSM-5 provides the specifier "with atypical features" for bipolar disorders that involve mood reactivity and at least two of the following: significant weight gain or increase in appetite, hypersomnia, leaden paralysis, interpersonal rejection sensitivity.
The depressive disorders include major depressive disorder, persistent depressive disorder, and disruptive mood dysregulation disorder.
Major depressive disorder requires five or more symptoms of a major depressive episode for at least two weeks with at least one symptom being depressed mood or loss of interest or pleasure in most or all activities.
Persistent depressive disorder requires a depressed mood with two or more characteristic symptoms (e.g., poor appetite or overeating, insomnia or hypersomnia, feelings of hopelessness) for at least two years in adults or one year in children and adolescents.
Disruptive mood dysregulation disorder requires the presence for at least 12 months of
(a) severe and recurrent temper outbursts that are verbal and/or behavioral, are grossly out of proportion to the situation or provocation, and occur three or more times each week; and
(b) a persistently irritable or angry mood that is observable to others most of the day and nearly every day between outbursts.
Specifiers provided in DSM-5 for major depressive disorder include with peripartum onset and with seasonal pattern:
-The specifier with peripartum onset applies when the onset of symptoms is during pregnancy or within four weeks after delivery. Up to 80% of women experience "baby blues" after the birth of their children and, according to DSM-5, about 3 to 6% have symptoms that are sufficiently severe to meet the criteria for a major depressive episode during pregnancy or the weeks or months following delivery. [Note that other sources report higher rates of major depressive disorder with peripartum onset, usually within the 10 to 20% range (e.g., English et al., 2018).]
-The specifier with seasonal pattern applies when there's a temporal relationship between mood episodes and time of year, which is usually winter. This disorder is also known as seasonal affective disorder (SAD), and its symptoms include hypersomnia, overeating, weight gain, and a craving for carbohydrates.
--It's been linked to a lower-than-normal level of serotonin and a higher-than-normal level of melatonin, which is a hormone that plays an essential role in the sleep-wake cycle. SAD is often responsive to phototherapy which involves exposure to bright light that suppresses the production of melatonin.
During childhood, the rates of depression are similar for boys and girls; however, the rate for females increases in early adolescence while the rate for males remains fairly stable.
-Explanations for this gender difference incorporate the impact of biological and psychological factors.
--For example, there's evidence that the increase of hormonal levels at puberty sensitizes females but desensitizes males to the stress of negative life events.
-The higher rate for females persists into adulthood, with female adolescents and adults having a rate that is 1.5 to 3 times higher than the rate for male adolescents and adults.
The yearly National Survey on Drug Use and Health (NSDUH), a nationally representative survey of U.S. adolescents and adults, provides information on the rates of one or more major depressive episodes in the past 12 months.
-From 2009 to 2017, the highest rates of depression (with three exceptions) were for respondents ages 12 to 17 followed by, in order, respondents ages 18 to 25, 26 to 49, and 50+.
--The exceptions were in 2009, 2010, and 2017: In 2009, respondents ages 12 to 17 and 18 to 25 had a similar rate; in 2010, respondents ages 18 to 25 had a slightly higher rate than those ages 12 to 17; and, in 2017, respondents ages 12 to 17 and 18 to 25 again had similar rates.
NSDUH data also indicate that rates of depression increased substantially between 2009 and 2017 for the two younger age groups but remained relatively stable for the two older age groups.
Major depressive disorder has been linked to heredity; neurotransmitter, hormone, and brain abnormalities; and cognitive and behavioral factors.
With regard to heredity, twin, family, and adoption studies have confirmed a genetic component.
-For example, twin studies have found that the concordance rate for unipolar depression is about .50 for monozygotic twins and .20 for dizygotic twins.
Major depressive disorder has also been linked to lower-than-normal levels of norepinephrine and serotonin and increased levels of cortisol in the hypothalamic-pituitary-adrenocortical (HPA) axis, which plays an important role in the body's reaction to stress.
-It's also associated with functional and structural abnormalities in several areas of the brain including the prefrontal cortex, cingulate cortex, hippocampus, caudate nucleus, putamen, amygdala, and thalamus.
--For example, with regard to the prefrontal cortex, functional brain imaging studies have found that (a) depression is associated with abnormally high levels of activity in the ventromedial prefrontal cortex (vmPFC) and abnormally low levels of activity in the dorsolateral prefrontal cortex (dlPFC) and (b) remission of depressive symptoms in response to psychotherapy or an antidepressant is associated with decreased activity in the vmPFC and increased activity in the dlPFC.
---In addition, studies using structural brain imaging techniques have linked depression to reduced volume of the orbitofrontal cortex, anterior cingulate cortex, hippocampus, putamen, and caudate nucleus.
Behavioral and cognitive explanations include Lewinsohn's social reinforcement theory, Seligman's learned helplessness model, and Beck's cognitive theory:
-Lewinsohn's (1974) social reinforcement theory describes depression as the result of a low rate of response-contingent reinforcement for social behaviors due to a lack of reinforcement in the environment and/or poor social skills.
--This results in social isolation, low self-esteem, pessimism, and other characteristics of depression that, in turn, further decrease the likelihood of positive reinforcement in the future.
-Seligman's (1974) original version of the learned helplessness model links depression to repeated exposure to uncontrollable negative life events that results in a sense of helplessness, and a reformulated version stresses the role of a negative cognitive style that involves attributing negative life events to stable, internal, and global factors.
--The most recent revision of the model (referred to as hopelessness theory) describes a sense of hopelessness as the proximal and sufficient cause of depression which, in turn, is the result of exposure to negative events and a negative cognitive style.
-Beck's (1974) cognitive theory attributes depression to a negative cognitive triad that consists of negative thoughts about oneself, the world, and the future.
There's evidence that risk factors for major depressive disorder are somewhat age-related.
-For example, for younger adults, the risk has been linked to genetics, stressful life events, and limitations in problem-solving and other cognitive abilities.
-In contrast, for older adults, chronic medical illness has been consistently identified as one of the strongest risk factors, especially when the illness decreases physical functioning and contributes to social isolation.
There's also evidence that the experience and expression of major depressive disorder are related to age and cultural background.
-With regard to age, older adults are less likely than younger adults to refer to affective symptoms and more likely to refer to somatic symptoms, cognitive changes, and a loss of interest in usual activities.
With regard to cultural background, members of some Latino, Mediterranean, Middle Eastern, Asian, and other non-Western cultures report a larger number of somatic symptoms than members of Western cultures who report a larger number of psychological symptoms.
-For example, Ryder and his colleagues (2008) compared Chinese and Euro-Canadian outpatients and found that the Chinese patients were more likely to emphasize somatic symptoms (e.g., appetite and sleep disturbances, headaches, heart palpitations), while Euro-Canadian patients were more likely to emphasize psychological symptoms (e.g., depressed mood, loneliness, hopelessness).
The treatment of major depressive disorder includes pharmacotherapy and/or psychosocial interventions.
Pharmacotherapy is often used for moderate and severe depression and depression that's recurrent or chronic and includes tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors (SNRIs), and other antidepressants.
Evidence-based psychosocial interventions include cognitive-behavior therapy, interpersonal therapy, behavioral activation therapy, problem-solving therapy, acceptance and commitment therapy, and emotion focused therapy.
There's also evidence that similar outcomes are obtained whether psychotherapy for depression is delivered via telepsychology or face-to-face.
Finally, bibliotherapy has been successfully used as an intervention for a number of disorders, with its effectiveness probably being best established for depression.
-For example, Gregory, Canning, Lee, and Wise (2004) conducted a meta-analysis of studies evaluating the effectiveness of cognitive bibliotherapy for adolescents and adults with this disorder.
-For 17 studies with a strong research design (pretest-posttest design with a wait list control group), these investigators obtained an effect size of .77 for individuals with mild to moderate depression, which is similar to the effect sizes reported in studies evaluating individual psychotherapy.
Suicide rates in the United States increased substantially between 1999 and 2017, with suicide being the 10th leading cause of death in 2017.
With regard to gender, the suicide rate for males was higher than the rate for females during this period.
-For example, in 2017, females ages 45 to 64 had the highest rate among females (9.7%), while males ages 75 and over had the highest rate among males (39.7%).
With regard to race/ethnicity, the suicide rate in 2017 was highest for American Indians/Alaska Natives followed by, in order, Whites, Asian/Pacific Islanders, Blacks, and Hispanics.
Finally, American Indians/Alaska Natives had the highest rates of suicide among individuals ages 15 to 24 and 25 to 44, while Whites had the highest rates among individuals ages 45 to 64 and 65 to 74
This diagnosis requires the presence of at least two of five characteristic symptoms for at least one month but less than six months, with at least one symptom being delusions, hallucinations, or disorganized speech.
The five characteristic symptoms are delusions, hallucinations, disorganized speech, grossly disorganized or catatonic behavior, and negative symptoms (e.g., avolition, alogia, anhedonia).
Schizophrenia has been linked to genetic factors and neurotransmitter and brain abnormalities.
-Evidence for a genetic contribution is provided by family studies which have found that, the greater the degree of genetic similarity, the greater the concordance rate (the likelihood that two people with shared genes will develop the same disorder).
The concordance rates for first-degree relatives reported by Gottesman (1991) are listed below:
Relationship to Person with Schizophrenia/Concordance Rate
Child of one parent with schizophrenia
Dizygotic (fraternal) twin
Child of two parents with schizophrenia
Monozygotic (identical) twin
Neurotransmitters that have been linked to schizophrenia include dopamine, glutamate, and serotonin.
-According to the original dopamine hypothesis, schizophrenia is due to high levels of dopamine or hyperactivity of dopamine receptors.
--Evidence for this hypothesis is provided by research showing that amphetamines increase dopamine activity and produce schizophrenia-like symptoms, while drugs that decrease dopamine activity reduce or eliminate these symptoms.
-A revised version of the dopamine hypothesis predicts that the positive symptoms of schizophrenia are due to dopamine hyperactivity in subcortical regions of the brain (especially in striatal areas), while the negative symptoms are due to dopamine hypoactivity in cortical regions (especially in the prefrontal cortex).
Brain abnormalities associated with schizophrenia include enlarged ventricles and hypofrontality, which refers to lower-than-normal activity in the prefrontal cortex and is believed to contribute to the disorder's negative and cognitive symptoms.
-One model of schizophrenia that's consistent with the revised dopamine hypothesis described above implicates cortical and subcortical regions.
--It predicts that dysfunction in the temporal-limbic-frontal network causes the negative symptoms of schizophrenia as well as disinhibition in subcortical areas of the brain that, in turn, increases the release of dopamine in the striatum (caudate nucleus, putamen, and nucleus accumbens) and causes the positive symptoms.
The psychotic symptoms of schizophrenia usually first appear between the late teens and early 30s, with the peak age of onset being in the early- to mid-20s for males and the late-20s for females.
Psychotic symptoms often decrease with increasing age, while negative symptoms and cognitive symptoms persist. A better prognosis for schizophrenia is associated with female gender, an acute and late onset of symptoms, comorbid mood symptoms (especially depressive symptoms), predominantly positive symptoms, precipitating factors, a family history of a mood disorder, and good premorbid adjustment. In contrast, anosognosia (a lack of insight into or awareness of one's disorder) is associated with non-adherence to treatment and an elevated risk for relapse. Patients whose family members are high in expressed emotion are also at increased risk for relapse. Expressed emotion refers to the emotional response of family members to a patient with schizophrenia or other mental disorder, and families high in expressed emotion are characterized by high levels of criticism and hostility toward and emotional overinvolvement with the patient (Butzlafff & Hooley, 1998).
The research has identified variations in the onset, course, and prognosis of schizophrenia across countries. For example, there's evidence that patients living in non-Western developing countries are more likely than those living in Western industrialized countries to experience an acute onset of symptoms, a shorter course, and a higher rate of remission (e.g., Hopper & Wanderling, 2000). The studies have also found that an "immigrant paradox" applies to schizophrenia, alcohol use disorder, and a number of other psychiatric disorders. It occurs when "newly arrived immigrants have better health outcomes than much more acculturated immigrants (with longer US residence) or even US born natives of the same ethnicity"
For this diagnosis, the person must have (a) deficits in intellectual functioning as determined by the results of a clinical assessment and a score that is about two standard deviations below the mean on an individualized, standardized intelligence test
(b) deficits in adaptive functioning that cause a failure to meet community standards of personal independence and social responsibility and impair functioning in one or more activities of daily life in multiple contexts
(c) an onset of the deficits during the developmental period.
A specifier is used to indicate level of severity (mild, moderate, severe, or profound), which is based on adaptive functioning in conceptual, social, and practical domains and is useful for determining the amount of support the person needs.
The cause of intellectual disability is known in 25 to 50% of all cases.
-Of cases with a known etiology, about 80 to 85% are due to prenatal factors (which includes chromosomal and other genetic causes), 5 to 10% are due to perinatal factors (e.g., asphyxia), and 5 to 10% are due to postnatal factors.
The most common chromosomal causes are Down's syndrome followed by fragile X syndrome, and the most common preventable prenatal cause is fetal alcohol syndrome
(a) persistent deficits in social communication and interaction in multiple contexts as indicated by deficits in social-emotional reciprocity, nonverbal communicative behaviors, and developing, maintaining, and understanding relationships
(b) restricted and repetitive patterns of behavior, interests, or activities as indicated by at least two of four symptoms:
-stereotyped or repetitive motor movements, use of objects, or speech
-insistence on sameness, inflexible adherence to routines, or ritualized patterns of verbal or nonverbal behavior
-highly restricted interests that are abnormal in intensity or focus
-hyper- or hyporeactivity to sensory input; and
(c) an onset of symptoms during the early developmental period that cause impairment in social, occupational, or other important area of functioning.
A specifier is used to indicate symptom severity as Level 1 (requiring support), Level 2 (requiring substantial support), or Level 3 (requiring very substantial support).
Associated features of ASD include intellectual and language impairment, self-injurious behaviors, motor deficits and abnormalities (e.g., catatonic-like behaviors), and disruptive/challenging behaviors.
Prognosis for this disorder is best when the person has an IQ over 70, functional language skills by age five, and an absence of comorbid mental health problems.
According to the DSM-5, reported frequencies for ASD in the United States and other countries approach 1% of the population, with frequencies being similar for children and adults.
With regard to gender, ASD is diagnosed four times more often in males than females.
The etiology of ASD is unknown in most cases, but the research suggests it has multiple causes.
-There's evidence that at least some cases are due to brain and/or neurotransmitter abnormalities.
--For example, the studies have linked ASD to structural abnormalities in the cerebellum and amygdala and a lower-than-normal level of serotonin synthesis that contributes to abnormal brain development.
--The studies have also linked ASD to higher-than-normal blood levels of serotonin, but the relationship between increased levels of serotonin in the blood and decreased serotonin synthesis in the brain is not well understood.
-Family, twin, and adoption studies support a genetic etiology.
-Finally, risk factors for ASD include male gender, family history of ASD, certain medical conditions (e.g., fragile X and Angelman syndromes), birth before 26 weeks of gestation, advanced parental age, and exposure to certain environmental toxins during prenatal development.
-Note that, despite extensive research, a link between ASD and childhood vaccinations has not been established (e.g., Hviid et al., 2019).
The primary goals for the treatment of children with ASD are to minimize the core symptoms of the disorder, maximize independence by promoting the acquisition of functional skills, and reduce or eliminate behaviors that may interfere with functional skills.
With regard to nonpharmacological interventions, early intensive behavioral intervention (EIBI) is an evidence-based treatment that uses the principles and techniques of applied behavior analysis (ABA).
-An example is Lovaas's (1987) method of EIBI, which involved providing young children with ASD with at least 40 hours per week of behavioral interventions and included using shaping and discrimination training to teach nonspeaking children to communicate verbally.
Research evaluating the outcomes of EIBI have found that it has the greatest positive impact on intelligence and language acquisition and a smaller and less consistent impact on adaptive skills, social functioning, and severity of core ASD symptoms (Weitlauf et al., 2014).
No medication has been found to be effective for the core symptoms of ASD, and medications are ordinarily prescribed for co-occurring psychiatric conditions and associated behaviors that cause distress but are not addressed by or haven't been alleviated by nonpharmacological interventions.
-For instance, methylphenidate and other psychostimulants are used to alleviate symptoms of ADHD; SSRIs are used to treat depression and anxiety; and atypical antipsychotics (especially risperidone and aripiprazole) are used to reduce irritability and aggressive, self-injurious, and other disruptive behaviors.
ADHD involves a pattern of inattention and/or hyperactivity-impulsivity that has persisted for at least six months, had an onset before 12 years of age, is present in at least two settings, and interferes with social, academic, or occupational functioning.
The diagnosis requires at least six symptoms of inattention and/or at least six symptoms of hyperactivity-impulsivity (or at least five symptoms for individuals age 17 and older).
Symptoms of inattention include doesn't listen when spoken to, fails to pay close attention to details, doesn't follow through on instructions, is easily distracted by extraneous stimuli, and is often forgetful in daily activities.
Symptoms of hyperactivity-impulsivity include is unable to engage in play or leisure activities quietly, often runs or climbs in inappropriate situations, talks excessively, has trouble waiting his/her turn, and interrupts or intrudes on others.
A specifier is used to indicate the subtype as predominantly inattentive presentation, predominantly hyperactive/impulsive presentation, or combined presentation.
ADHD is twice as common in males than females during childhood but the gender difference decreases somewhat in adulthood when the ratio of males to females is about 1.6:1.
Up 80% of school-age children with ADHD continue to meet the diagnostic criteria for the disorder in adolescence, and up to 30% continue to do so into adulthood.
-However, symptoms tend to vary over the lifespan, with overactivity decreasing the most during adolescence and adulthood, inattention decreasing slightly during adolescence and adulthood, and impulsivity decreasing slightly and changing in adulthood to include such behaviors as driving recklessly and abruptly quitting a job or ending a relationship.
Children with ADHD have high rates of comorbidity. Although the reported rates of specific comorbid disorders vary somewhat, most studies have found oppositional defiant disorder to be the most common comorbid disorder followed by, in order, conduct disorder, an anxiety disorder, and a depressive disorder.
ADHD has been linked to a number of brain abnormalities.
-Structural neuroimaging studies have found that overall brain volume and the volumes of the caudate nucleus, putamen, nucleus accumbens, amygdala, and hippocampus are smaller in people with ADHD.
-In addition, children and adolescents with this disorder have delayed cortical maturation (especially in the prefrontal cortex), while adults have reduced cortical thickness.
Functional neuroimaging studies have identified hyper- or hypoactivation in several brain networks.
-For example, these studies have found that children with ADHD often exhibit hypoactivation in the frontoparietal network, which consists of the dorsolateral and anterior prefrontal cortex, anterior cingulate cortex, lateral cerebellum, caudate nucleus, and inferior parietal lobe.
ADHD has also been linked to abnormalities in dopamine, norepinephrine, and serotonin activity.
A genetic contribution has been confirmed by the results of family, twin, and adoption studies which indicate that ADHD is one of the most heritable of all psychiatric disorders.
-For example, twin studies suggest a genetic contribution in about 76% of cases.
-In addition, there's evidence that ADHD shares the same inherited genetic variations with major depressive disorder, bipolar disorder, schizophrenia, and autism spectrum disorder.
ADHD has also been linked to low birth weight, premature birth, and maternal smoking or alcohol use during pregnancy.
Finally, Barkley (1997) describes the proximal cause of ADHD to be a deficit in behavioral inhibition which affects four executive neurocognitive functions that depend on behavioral inhibition:
-internalization of speech
-self-regulation of affect, motivation, and arousal
-reconstitution (behavioral analysis and synthesis).
--In turn, these functions influence the motor system that controls goal-directed behavior.
The best treatment for ADHD depends, to some degree, on the person's age.
For example, guidelines prepared by American Academy of Pediatrics (2011) recommend
(a) parent and teacher administered behavioral interventions as the treatment-of-choice for preschool-aged children and medication (methylphenidate) only when behavioral interventions are inadequate;
(b) a combination of behavioral interventions and medication for elementary school-aged children, and
(c) medication for adolescents with their assent or, preferably, medication plus behavior therapy.
The DSM-5 defines a tic as a "sudden, rapid, recurrent, nonrhythmic motor movement or vocalization".
Motor tics include eye blinking, facial grimacing, shoulder shrugging, and echopraxia, while vocal tics include throat clearing, barking, and echolalia.
The DSM-5 distinguishes between three tic disorders:
-Tourette's disorder requires at least one vocal tic and multiple motor tics that may occur together or at different times, may wax and wane in frequency but have persisted for more than one year, and had an onset before 18 years of age.
-Persistent (chronic) motor or vocal tic disorder requires one or more motor or vocal tics that have persisted for more than one year and began before age 18.
-Provisional tic disorder requires one or more motor and/or vocal tics that have been present for less than one year and began before age 18.
The onset of tics is typically between four and six years of age, and the severity of tics ordinarily peaks between 10 and 12 years of age.
Tourette's disorder has been linked to dopamine overactivity, a smaller-than-normal caudate nucleus, and heredity.
Treatment may include an antipsychotic drug (e.g., haloperidol) and medication for comorbid conditions - e.g., serotonin for obsessive-compulsive symptoms and methylphenidate or clonidine for ADHD.
Behavioral treatments include comprehensive behavioral intervention for tics (CBIT), which consists of psychoeducation, social support, and habit reversal, competing response, and relaxation training.
These disorders involve deficits in language, speech, and communication. Included in this category is:
Childhood-onset fluency disorder (stuttering), which involves a disturbance in normal fluency and time patterning of speech that's inappropriate for the person's age and language skills, persists over time, and includes one or more of seven symptoms: sound and syllable repetitions, sound prolongations, broken words, audible or silent blocking, circumlocutions, words pronounced with excessive physical tension, monosyllabic whole-word repetitions.
The onset is usually between two and seven years of age. Sixty-five to 85% of children recover from dysfluency, with the severity of symptoms at age eight being a good predictor of persistence or recovery.
The treatment-of-choice is habit reversal training which incorporates several strategies including competing response training that, for this disorder, is regulated breathing.
requires difficulties related to academic skills as indicated by the presence of at least one of six symptoms that last for at least six months despite the use of interventions that address difficulties:
-inaccurate or slow and effortful word reading
-difficulty understanding the meaning of what is read
-difficulties with spelling
-difficulties with written expression
-difficulties mastering number sense, number facts, or calculation
-difficulties with mathematical reasoning.
For the diagnosis, the person's academic skills must be substantially below those expected for his/her age, interfere with academic or occupational performance or activities of daily living, have an onset during the school-age years, and not be better accounted for by another disorder or condition (e.g., uncorrected visual or auditory impairment).
Specifiers are used to indicate subtype (with impairment in reading, with impairment in written expression, or with impairment in mathematics) and level of severity.
About 5 to 15 percent of school-age children have a specific learning disability and approximately 80% of these children have a reading disorder.
Of the reading disorders, dyslexia is the most common type; of the types of dyslexia, dysphonic dyslexia is most common.
-It involves difficulties connecting sounds to letters and is also known as dysphonetic, auditory, and phonological dyslexia.
People with a specific learning disorder usually have an average to above-average IQ but elevated rates of other problems and disorders (especially ADHD).
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