Major depressive episode

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Major_depressive_episode 

Major depressive episode
Specialty	Psychiatry

A major depressive episode (MDE) is a period characterized by the symptoms of major depressive disorder. Those affected primarily have a depressed mood for at least two weeks or more and a loss of interest or pleasure in everyday activities. Other symptoms can include feelings of emptiness, hopelessness, anxiety, worthlessness, guilt, irritability, changes in appetite, problems concentrating, remembering details, making decisions, and thoughts of suicide. Insomnia or hypersomnia, aches, pains, or digestive problems that are resistant to treatment may also be present.

Although the exact origin of depression is still not clear, it is believed to involve biological, psychological, and social aspects. Factors like socioeconomic status, life experience, genetics, and personality tendencies play a role in the development of depression and may represent an increased risk of developing a major depressive episode. There are many theories as to how depression occurs. One interpretation is that neurotransmitters in the brain are out of balance, resulting in feelings of worthlessness and despair. Magnetic resonance imaging shows that the brains of people who have depression look different than the brains of people who do not exhibit signs of depression. A family history of depression increases the chance of being diagnosed.

Emotional pain and economic costs are associated with depression in many cases. In the United States and Canada, the costs associated with major depression are comparable to those related to heart disease, diabetes, and back problems and are greater than the costs of hypertension. According to the Nordic Journal of Psychiatry, there is a direct correlation between a major depressive episode and unemployment.

Treatments for a major depressive episode include psychotherapy and antidepressants, although in more serious cases, hospitalization or intensive outpatient treatment may be required.

Signs and symptoms

The criteria below are based on the formal DSM-5 criteria for a major depressive episode. A diagnosis of a major depressive episode requires the patient to have experienced five or more of the symptoms below, one of which must be either a depressed mood or a loss of interest or pleasure (although both are frequently present). These symptoms must be present for at least 2 weeks and represent a change from the patient's normal behavior.

Depressed mood and loss of interest (anhedonia)

Either a depressed mood or a loss of interest or pleasure must be presented for the diagnosis of a major depressive episode. Depressed mood is the most common symptom seen in major depressive episodes. Interest in or pleasure in everyday activities can be decreased; this is referred to as anhedonia. These feelings must be present on an everyday basis for two weeks or longer to meet the DSM-V criteria for a major depressive episode. In addition, the person may experience one or more of the following emotions: sadness, emptiness, hopelessness, indifference, anxiety, tearfulness, pessimism, emotional numbness, or irritability. In children and adolescents, a depressed mood often appears more irritable. There may be a loss of interest in or desire for sex or other activities once found to be pleasant. Friends and family of the depressed person may notice that they have withdrawn from friends, neglected them, or quit doing activities that were once a source of enjoyment.

Sleep

Major depressive episodes are known to cause sleep disturbances such as hypersomnia, which causes excessive sleep patterns, or sleep deprivation, like insomnia. Insomnia is the most common type of sleep disturbance for people who are clinically depressed. Symptoms of insomnia include trouble falling asleep, trouble staying asleep, or waking up too early in the morning. The most common symptom of insomnia is waking up in the middle of the night and having trouble falling back asleep. Hypersomnia is a less common type of sleep disturbance. It may include sleeping for prolonged periods at night and into the morning or increased sleeping during the daytime. The sleep may not be restful, and the person may feel sluggish despite many hours of sleep, which may amplify their depressive symptoms and interfere with other aspects of their lives. This type of sleep disorder may make it harder for a person to fall and stay asleep at night compared to during the day. Hypersomnia is often associated with atypical depression as well as seasonal affective disorder.

Feelings of guilt or worthlessness

Depressed people may have feelings of guilt that go beyond a normal level or be delusional. These feelings of guilt and/or worthlessness are excessive and imagined. Major depressive episodes are notable for a significant, often inexplicable, drop in self-esteem. The guilt and worthlessness experienced in a major depressive episode can range from subtle feelings of guilt to frank delusions, shame, and humiliation. Additionally, self-loathing is common in clinical depression and can lead to a downward spiral when combined with other symptoms. A lot of people with depression have distorted thought patterns, and genuinely believe that they're not good for anything or anyone. They tend to have severe self-esteem issues, and don't recognize their value as a human being. They also begin to feel as though their lives have no meaning or purpose.

Loss of energy

Individuals going through a major depressive episode often have a general lack of energy, as well as fatigue and tiredness, nearly every day for at least 2 weeks. A person may feel tired without having engaged in any physical activity, and day-to-day tasks become increasingly difficult. It becomes very difficult for someone with depression to get things done during the day. Even small tasks, like showering, become exhausting, causing a lot of people with depression to stop taking care of themselves entirely.

Decreased concentration

Nearly every day, the person may be indecisive or have trouble thinking or concentrating. These issues cause significant difficulty in functioning for those involved in intellectually demanding activities, such as school and work, especially in difficult fields. Depressed people often describe a slowing of thought, an inability to concentrate and make decisions, and being easily distracted. In the elderly, the decreased concentration caused by a major depressive episode may present as deficits in memory. This is referred to as pseudodementia and often goes away with treatment. Decreased concentration may be reported by the patient or observed by others. Since depression makes it more difficult to stay concentrated, a lot of people will notice that they aren't doing well in school or at their job, which makes their depression even worse.

Change in eating, appetite, or weight

In a major depressive episode, appetite is most often decreased, although a small percentage of people experience an increase in appetite. A person experiencing a depressive episode may have a marked loss or gain of weight (5% of their body weight in one month). A decrease in appetite may result in unintentional weight loss when a person is not dieting. Feelings of low self-worth make them not want to eat anymore. Some people experience an increase in appetite and may gain significant amounts of weight. They may crave certain types of food, such as sweets or carbohydrates. In this instance, low self-worth can lead to self-soothing through eating. In children, failure to make expected weight gains may be counted towards this criteria. Overeating is often associated with atypical depression. When people have depression, they usually stop taking care of their bodies and "wither away." A lack of healthy eating habits is a tell-tale sign of classic depression.

Motor activity

Nearly every day, others may see that the person's activity level is not normal. They might notice that the person takes longer to complete simple tasks or that they are doing a lot at once. People with depression may be overly active (psychomotor agitation) or very lethargic (psychomotor retardation). Psychomotor agitation is marked by an increase in body activity, which may result in restlessness, an inability to sit still, pacing, hand wringing, or fidgeting with clothes or objects. This could also be linked to anxiety, since depression and anxiety are often seen together. Psychomotor retardation results in a decrease in body activity or thinking. In this case, a depressed person may demonstrate a slowing of thinking, speaking, or body movement. They may speak more softly or say less than usual. This is because they do not have the energy to expend as a normal person would. To meet diagnostic criteria, changes in motor activity must be so abnormal that it can be observed by others. Personal reports of feeling restless or slow do not count towards the diagnostic criteria.

Thoughts of death and suicide

A person going through a major depressive episode may have repeated thoughts about death (other than the fear of dying) or suicide (with or without a plan), or may have made a suicide attempt. Suicidal ideation can be common amongst victims of depression, which is when a person often thinks about not being alive anymore but does not yet have a plan to carry it out. The frequency and intensity of thoughts about suicide can range from believing that friends and family would be better off if one were dead to frequent thoughts about committing suicide (generally related to wishing to stop the emotional pain) to detailed plans about how the suicide would be carried out. Those who are more severely suicidal may have made specific plans and decided upon a day and location for the suicide attempt. When this happens, they often keep to themselves about it and may do it when and where they think no one would suspect.

Comorbid disorders

Major depressive episodes may show comorbidity (association) with other physical and mental health problems. About 20–25% of individuals with a chronic general medical condition will develop major depression. Common comorbid disorders include eating disorders, substance-related disorders, panic disorder, and obsessive-compulsive disorder. Up to 25% of people who experience a major depressive episode have a pre-existing dysthymic disorder.

Some people who have a fatal illness or are at the end of their lives may experience depression, although this is not universal.

Causes

The cause of a major depressive episode is not well understood. Despite its longstanding prominence in pharmaceutical advertising, the myth that low serotonin levels cause depression is not supported by scientific evidence. There are usually many factors that play into a person's depression. The mechanism is believed to be a combination of biological, psychological, and social factors. A major depressive episode can often follow an acute stress in someone's life, such as the death of a loved one, or being fired from a job. Evidence suggests that psychosocial stressors play a larger role in the first 1–2 depressive episodes, while having less influence in later episodes. People who experience a major depressive episode often have other mental health issues.

Other risk factors for a depressive episode include:

• Early childhood trauma
• Family history of a mood disorder
• Lack of interpersonal relationships
• Personality (insecure, worried, stress-sensitive, obsessive, unassertive, dependent)
• Postpartum
• Recent negative life events

Studies show that depression can be passed down in families, but this is believed to be due to a combined effect of genetic, and environmental factors. Other medical conditions, like hypothyroidism, for example, may cause people to experience similar symptoms as a major depressive episode, however this would be considered a mood disorder due to a general medical condition, according to the DSM-V. For some people, depression runs in their family so it's likely that the depression will be passed down to them. For other people, depression might be completely environmental. It could also be a mix of both.

Diagnosis

Criteria

The two main symptoms of a major depressive episode are a depressed mood and a loss of interest or pleasure. From the list below, one bold symptom and four other symptoms must be presented for at least 2 weeks for a diagnosis of a major depressive episode. These symptoms must be causing significant distress or impairment in functioning.

• Change in appetite
• Change in body activity (psychomotor changes)
• Change in sleep
• Depressed mood
• Feelings of worthlessness and excessive or inappropriate guilt
• Indecisiveness, confusion, or a decrease in concentration
• Loss of energy
• Loss of interest or pleasure
• Suicidal ideation

To diagnose a major depressive episode, a trained healthcare provider must make sure that:

• The symptoms are not due to any direct physiological effect of a substance (e.g., abuse of a drug or medication) or a general medical condition (e.g., hypothyroidism).
• The symptoms do not meet the criteria for a mixed episode.
• The symptoms must cause considerable distress or impair functioning at work, in social settings, or in other important areas to qualify as an episode.

Workup

No labs are diagnostic of a depressive episode. But some labs can help rule out general medical conditions that may mimic the symptoms of a depressive episode. Healthcare providers may order some routine blood work, including routine blood chemistry, CBC with differential, thyroid function studies, and Vitamin B12 levels, before making a diagnosis.

Differential diagnosis

There are other mental health disorders or medical conditions to consider before diagnosing a major depressive episode: A doctor or psychiatrist should consider these options before making a definitive diagnosis, in order to avoid misdiagnosing a patient.

• Adjustment disorder
• Anxiety disorder (Generalized anxiety, PTSD, obsessive-compulsive disorder)
• Bipolar disorder
• Cyclothymic disorder
• Depression due to a general medical condition
• Disruptive mood dysregulation disorder
• Gender dysphoria
• Persistent depressive disorder
• Personality disorder with depressive symptoms
• Premenstrual dysphoric disorder
• Substance abuse or Substance use disorder

Screening

Healthcare providers may screen patients in the general population for depression using a screening tool, such as the Patient Healthcare Questionnaire-2 (PHQ-2). If the PHQ-2 screening is positive for depression, a provider may then administer the PHQ-9. The Geriatric Depression Scale is a screening tool that can be used in the elderly population.

Treatment

Depression is a treatable illness. Treatments for a major depressive episode may be provided by mental health specialists (i.e. psychologists, psychiatrists, social workers, counselors, etc.), mental health centers or organizations, hospitals, outpatient clinics, social service agencies, private clinics, peer support groups, clergy, and employee assistance programs. The treatment plan could include psychotherapy alone, antidepressant medications alone, or a combination of medication and psychotherapy.

For major depressive episodes of severe intensity (multiple symptoms, minimal mood reactivity, severe functional impairment), combined psychotherapy, and antidepressant medications are more effective than psychotherapy alone. Meta-analyses suggest that the combination of psychotherapy and antidepressant medications is more effective in treating mild and moderate forms of depression as well, compared to either type of treatment alone. Patients with severe symptoms may require outpatient treatment or hospitalization.

The treatment of a major depressive episode can be split into 3 phases:

1. Acute phase: the goal of this phase is to resolve the current major depressive episode
2. Continuation: this phase continues the same treatment from the acute phase for 4–8 months after the depressive episode has resolved and the goal is to prevent relapse
3. Maintenance: this phase is not necessary for every patient but is often used for patients who have experienced 2–3 or more major depressive episodes. Treatment may be maintained indefinitely to prevent the occurrence and severity of future episodes.

Therapy

Psychotherapy, also known as talk therapy, counseling, or psychosocial therapy, is characterized by a patient talking about their condition and mental health issues with a trained therapist. Therapy alone has been proven to benefit people who are struggling with various mental illnesses. Different types of psychotherapy are used as a treatment for depression. These include cognitive behavioral therapy, interpersonal therapy, dialectical behavior therapy, acceptance and commitment therapy, and mindfulness techniques. Evidence shows that cognitive behavioral therapy can be as effective as medication in the treatment of a major depressive episode.

Psychotherapy may be the first treatment used for mild to moderate depression, especially when psychosocial stressors are playing a large role. Psychotherapy alone may not be as effective for more severe forms of depression, such as depression where there's a chemical imbalance in the brain.

Some of the main forms of psychotherapies used for the treatment of a major depressive episode, along with what makes them unique are included below:

• Cognitive psychotherapy: focus on patterns of thinking
• Interpersonal psychotherapy: focus on relationships, losses, and conflict resolution
• Problem-solving psychotherapy: focus on situations and strategies for problem-solving
• Psychodynamic psychotherapy: focus on defense mechanisms and coping strategies

Medication

Prozac is one example of an SSRI, the class of antidepressant medications that are used as the first line in the treatment of depression.

Medications used to treat depression include selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), norepinephrine-dopamine reuptake inhibitors (NDRIs), tricyclic antidepressants, monoamine oxidase inhibitors (MAOIs), and atypical antidepressants such as mirtazapine, which do not fit neatly into any of the other categories. Different antidepressants work better for different individuals, it simply comes down to the person and what they prefer. It is often necessary to try several before finding one that works best for a specific patient. Some people may find it necessary to combine medications, which could mean two antidepressants or an antipsychotic medication in addition to an antidepressant. If a person's close relative has responded well to a certain medication, that treatment will likely work well for him or her. For example, if the depression is familial and the person's mother is prescribed an SSRI, then the same SSRI will most likely benefit the person as well. Antidepressant medications are effective in the acute, continuation, and maintenance phases of treatment, as described above.

The treatment benefits of antidepressant medications are often not seen until 1–2 weeks into treatment, with maximum benefits being reached around 4–6 weeks. It is likely that the person will actually experience more negative side effects during the first week or two, and want to stop taking their medication. However, it is crucial that they push through until the 4–6-week mark to know for sure how they feel about it. Most healthcare providers will monitor patients more closely during the acute phase of treatment and continue to monitor them at longer intervals in the continuation and maintenance phases.

Sometimes, people stop taking antidepressant medications due to side effects, although side effects often become less severe over time. Suddenly stopping treatment or missing several doses may cause withdrawal-like symptoms. Some studies have shown that antidepressants may increase short-term suicidal thoughts or actions, especially in children, adolescents, and young adults. However, antidepressants are more likely to reduce a person's risk of suicide in the long run.

Below are listed the main classes of antidepressant medications, some of the most common drugs in each category, and their major side effects:

• Monoamine oxidase inhibitors (isocarboxazid, phenelzine, selegiline): major side effects include high blood pressure (emergency) if eaten with foods rich in tyramine (e.g. cheeses, some meats, and home-brewed beer), sedation, tremor, and orthostatic hypotension
• Selective serotonin reuptake inhibitors (citalopram, escitalopram, paroxetine, fluoxetine, sertraline): major side effects include nausea, diarrhea, and sexual dysfunction such as erectile dysfunction or anorgasmia
• Serotonin and norepinephrine reuptake inhibitors (duloxetine, venlafaxine, desvenlafaxine): major side effects include nausea, diarrhea, increased heart rate, increased blood pressure, and tremors
• Tricyclic antidepressants (amitryptiline, desipramine, doxepin, imipramine, nortriptyline): major side effects include sedation, low blood pressure when moving from sitting to standing (orthostatic hypotension), tremor, and heart issues like conduction delays or arrhythmias

Alternative treatments

There are several treatment options that exist for people who have experienced several episodes of major depression or have not responded to several treatments.

Electroconvulsive therapy is a treatment in which a generalized seizure is induced by means of electrical current. The mechanism of action of the treatment is not clearly understood but has been shown to be most effective in the most severely depressed patients. For this reason, electroconvulsive therapy is preferred for the most severe forms of depression or depression that has not responded to other treatments, known as refractory depression.

Vagus nerve stimulation is another alternative treatment that has been proven to be effective in the treatment of depression, especially people that have been resistant to four or more treatments. Some of the unique benefits of vagus nerve stimulation include improved neurocognitive function and a sustained clinical response.

Transcranial magnetic stimulation is also an alternative treatment for a major depressive episode. It is a non-invasive treatment that is easily tolerated and shows an antidepressant effect, especially in more typical depression and younger adults.

Prognosis

If left untreated, a typical major depressive episode may last for several months. About 20% of these episodes can last two years or more. About half of depressive episodes end spontaneously. However, even after the major depressive episode is over, 20% to 30% of patients have residual symptoms, which can be distressing and associated with disability. Fifty percent of people will have another major depressive episode after the first. However, the risk of relapse is decreased by taking antidepressant medications for more than 6 months.

Symptoms completely improve in six to eight weeks in sixty to seventy percent of patients. The combination of therapy and antidepressant medications has been shown to improve resolution of symptoms and outcomes of treatment.

Suicide is the 8th leading cause of death in the United States. The risk of suicide is increased during a major depressive episode. However, the risk is even more elevated during the first two phases of treatment. There are several factors associated with an increased risk of suicide, listed below:

• Alcohol or drug use or comorbid psychiatric disorder
• Detailed plan
• Family history of suicide or mental illness
• Greater than 45 years of age
• History of suicide attempt or self-injurious behaviors
• Inability to accept help
• Lack of social support
• Male
• Poor health
• Psychotic features (auditory or visual hallucinations, disorganization of speech, behavior, or thought)
• Recent severe loss
• Severe depression

Epidemiology

Estimation of the number of people with major depressive episodes and major depressive disorder (MDD) vary significantly. Overall, 13–20% of people will experience significant depressive symptoms at some point in their life. The overall prevalence of MDD is slightly lower ranging from 3.7 to 6.7% of people. In their lifetime, 20% to 25% of women, and 7% to 12% of men will have a major depressive episode. The peak period of development is between the ages of 25 and 44 years. Onset of major depressive episodes or MDD often occurs to people in their mid-20s, and less often to those over 65. The prevalence of depressive symptoms in the elderly is around 1–2%. Elderly persons in nursing homes may have increased rates, up to 15–25%. African-Americans have higher rates of depressive symptoms compared to other races. Prepubescent girls are affected at a slightly higher rate than prepubescent boys.

In a National Institute of Mental Health study, researchers found that more than 40% of people with post-traumatic stress disorder had depression four months after the traumatic event they experienced.

Women who have recently given birth may be at increased risk for having a major depressive episode. This is referred to as postpartum depression and is a different health condition than the baby blues, a low mood that resolves within 10 days after delivery.

Mood swing

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Mood_swing

 

Graphical comparison of mood swings, compared with bipolar disorder and cyclothymia

A mood swing is an extreme or sudden change of mood. Such changes can play a positive part in promoting problem solving and in producing flexible forward planning, or be disruptive. When mood swings are severe, they may be categorized as part of a mental illness, such as bipolar disorder, where erratic and disruptive mood swings are a defining feature.

Overview

Speed and extent

Mood swings can happen any time at any place, varying from the microscopic to the wild oscillations of bipolar disorder, so that a continuum can be traced from normal struggles around self-esteem, through cyclothymia, up to a depressive disease. However most people's mood swings remain in the mild to moderate range of emotional ups and downs. The duration of bipolar mood swings also varies. They may last a few hours – ultrarapid – or extend over days – ultradian: clinicians maintain that only when four continuous days of hypomania, or seven days of mania, occur, is a diagnosis of bipolar disorder justified. In such cases, mood swings can extend over several days, even weeks: these episodes may consist of rapid alternation between feelings of depression and euphoria.

Causes

There can be many different causes for mood swings. Some mood swings can be classified as normal/healthy reactions, such as grief processing, adverse effects of substances/drugs, or a result of sleep deprivation. Mood swings can also be a sign of psychiatric illnesses in the absence of external triggers or stressors.

Changes in a person's energy level, sleep patterns, self-esteem, sexual function, concentration, drug or alcohol use can be signs of an oncoming mood disorder.

Other major causes of mood swings (besides bipolar disorder and major depression) include diseases/disorders which interfere with nervous system function. Attention deficit hyperactivity disorder (ADHD), epilepsy, and autism spectrum are three such examples.

The hyperactivity sometimes accompanied by inattentiveness, impulsiveness, and forgetfulness are cardinal symptoms associated with ADHD. As a result, ADHD is known to bring about usually short-lived (though sometimes dramatic) mood swings. The communication difficulties associated with autism, and the associated changes in neurochemistry, are also known to cause autistic fits (autistic mood swings). The seizures associated with epilepsy involve changes in the brain's electrical firing, and thus may also bring about striking and dramatic mood swings. If the mood swing is not associated with a mood disorder, treatments are harder to assign. Most commonly, however, mood swings are the result of dealing with stressful and/or unexpected situations in daily life.

Degenerative diseases of the human central nervous system such as Parkinson's disease, Alzheimer's disease, multiple sclerosis, and Huntington's disease may also produce mood swings. Celiac disease can also affect the nervous system and mood swings can appear.

Not eating on time can contribute, or eating too much sugar, can cause fluctuations in blood sugar, which can cause mood swings.

Brain chemistry

If a person has an abnormal level of one or several of certain neurotransmitters (NTs) in their brain, it may result in having mood swings or a mood disorder. Serotonin is one such neurotransmitter that is involved with sleep, moods, and emotional states. A slight imbalance of this NT could result in depression. Norepinephrine is a neurotransmitter that is involved with learning, memory, and physical arousal. Like serotonin, an imbalance of norepinephrine may also result in depression.

List of conditions known to cause mood swings

• Anabolic steroid abuse
• Attention deficit hyperactivity disorder
• Autism or other pervasive developmental disorder
• Bipolar disorder or cyclothymia
• Borderline personality disorder
• Dementia, including Alzheimer's disease, Parkinson's disease and Huntington's disease
• Dopamine dysregulation syndrome
• Epilepsy
• Hypothyroidism or hyperthyroidism
• Intermittent explosive disorder
• Menopause
• Major depression
• Post traumatic stress disorder
• Pregnancy
• Premenstrual syndrome
• Schizoaffective disorder
• Schizophrenia
• Seasonal affective disorder
• XXYY syndrome

Treatment

Cognitive behavioral therapy recommends using emotional dampeners to break the self-reinforcing tendencies of either manic or depressive mood swings. Exercise, treats, seeking out small (and easily attainable) triumphs, and using vicarious distractions like reading or watching TV, are among the techniques found to be regularly used by people in breaking depressive swings.

Learning to bring oneself down from grandiose states of mind, or up from exaggerated shame states, is part of taking a proactive approach to managing one's own moods and varying sense of self-esteem.

Cyclothymia

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Cyclothymia 

 

Cyclothymia
Other names	Cyclothymic disorder, psychothemia, psychothymia, bipolar III, affective personality disorder, cyclothymic personality disorder
Specialty	Psychiatry, clinical psychology
Symptoms	Periods of depression and elevated mood
Complications	Suicide, self-harm
Causes	Unknown
Risk factors	Family history
Differential diagnosis	Bipolar disorder, borderline personality disorder, substance misuse disorder
Treatment	Psychotherapy, medications
Frequency	0.4–1% at some point in life

Cyclothymia (/ˌsaɪkləˈθaɪmiə/ siy-kluh-THIY-mee-uh), also known as cyclothymic disorder, psychothemia / psychothymia, bipolar III, affective personality disorder and cyclothymic personality disorder, is a mental and behavioural disorder that involves numerous periods of symptoms of depression and periods of symptoms of elevated mood. These symptoms, however, are not sufficient to indicate a major depressive episode or a manic episode. Symptoms must last for more than one year in children and two years in adults.

The cause of cyclothymia is unknown. Risk factors include a family history of bipolar disorder. Cyclothymia differs from bipolar in that major depression and mania are not found.

Treatment is generally achieved with counseling and mood stabilizers such as lithium. It is estimated that 0.4–1% of people have cyclothymia at some point in their life. The disorder's onset typically occurs in late childhood to early adulthood. Males and females are affected equally often.

Symptoms

People with cyclothymia experience both depressive phases and hypomanic phases (which are less severe than full manic episodes). The depressive and hypomanic symptoms in cyclothymia last for variable amounts of time due to the unstable and reactive nature of the disorder. The depressive phases are similar to major depressive disorder and are characterized by dulled thoughts and sensations and the lack of motivation for intellectual or social activities. Most people with cyclothymia are generally fatigued and tend to sleep frequently and for long periods of time. However, other people experience insomnia.

Other symptoms of cyclothymic depression include indifference toward people or activities that used to be extremely important. Cyclothymic depression also leads to difficulty making decisions. In addition, people with this condition tend to be critical and complain easily. Suicidal thoughts are common, even in mild forms of cyclothymia. In the depressive state, people with cyclothymia also experience physical complaints including frequent headaches, tightness in the head and chest, an empty sensation in the head, weakness, weight loss, and hair loss.

The distinguishing factor between typical depression and cyclothymic depression is that in cyclothymic depression, there are instances of hypomania. People with cyclothymia can switch from the depressive state to the hypomanic state without warning to them or others. The duration and frequency of phases is unpredictable.

In the hypomanic state, people's thoughts become faster and they become more sociable and talkative. They may engage in spending sprees, spontaneous actions, have heightened self-esteem, and greater vanity. In contrast to a regular manic state that would be associated with bipolar I, symptoms in the hypomanic phase generally occur in a less severe form.

Cyclothymia commonly occurs in conjunction with other disorders. Between 20 and 50 percent of people with depression, anxiety, and related disorders also have cyclothymia. When people with cyclothymia seek mental health resources it tends to be for symptoms of their comorbid condition rather than for their symptoms of cyclothymia. In children and adolescents, the most common comorbidities with cyclothymia are anxiety disorders, impulse control issues, eating disorders, and ADHD. In adults, cyclothymia also tends to be comorbid with impulse control issues. Sensation-seeking behaviors occur in hypomanic states.

In addition to sensation-related disorders, cyclothymia has also been associated with atypical depression. In one study, a connection was found between interpersonal sensitivity, mood reactivity (i.e., responding to actual or potential positive events with brighter mood), and cyclothymic mood swings, all of which are symptoms of atypical depression. Cyclothymia also tends to occur in conjunction with separation anxiety, where a person has anxiety as a result of separation from a caregiver, friend, or loved one. Other issues that tend to co-occur with cyclothymia include social anxiety, fear of rejection and a tendency toward hostility to those connected with past pain and rejection. People with cyclothymia tend to seek intense interpersonal relationships when in a hypomanic state and isolation when in a depressed state. This generally leads to short, tumultuous relationships.

Causes

The cause is unknown. Risk factors include a family history of bipolar disorder.

First-degree relatives of people with cyclothymia have major depressive disorder, bipolar I disorder, and bipolar II disorder more often than the general population. Substance-related disorders also may be at a higher risk within the family. First-degree relatives of a bipolar I individuals may have a higher risk of cyclothymic disorder than the general population.

Diagnosis

Cyclothymia is classified in DSM-5 as a subtype of bipolar disorder. The criteria are:

1. Periods of elevated mood and depressive symptoms for at least half the time during the last two years for adults and one year for children and teenagers.
2. Periods of stable moods last only two months at most.
3. Symptoms create significant problems in one or more areas of life.
4. Symptoms do not meet the criteria for bipolar disorder, major depression, or another mental disorder.
5. Symptoms are not caused by substance use or a medical condition.

The DSM-5 criteria for cyclothymia are restrictive according to some researchers. This affects the diagnosis of cyclothymia because fewer people get diagnosed than potentially could. This means that a person who has some symptoms of the disorder might not be able to get treatment because they do not meet all of the necessary criteria described in DSM-5. Furthermore, it also leads to more attention being placed on depression and other bipolar-spectrum disorders because if a person does not meet all the criteria for cyclothymia they are often given a depression or bipolar spectrum diagnosis. Improper diagnosis may lead some people with cyclothymia to be treated for a comorbid disorder rather than having their cyclothymic tendencies addressed.

Cyclothymia is often not recognized by the affected individual or medical professionals due to its ostensibly mild symptoms. In addition, it is difficult to identify and classify. Due to disagreement and misconceptions among health and mental health professionals, cyclothymia is often diagnosed as "bipolar not otherwise specified". Cyclothymia is also often confused with borderline personality disorder due to their similar symptoms, especially in older adolescents and young adults.

Most people with the disorder present in a depressive state, not realizing that their hypomanic states are abnormal. Mild manic episodes tend to be interpreted as part of the person's personality or simply a heightened mood. In addition, the disorder often manifests during childhood or adolescence, making it even more difficult for the person to distinguish between symptoms of the disorder and their personality. For example, people may think that they just have mood swings and not realize that these are a result of a psychiatric condition.

Management

Cognitive behavioral therapy (CBT) is considered potentially effective for people diagnosed with cyclothymia.

Medication can be used in addition to behavioral approaches. However, mood stabilizers should be used before antidepressants, and if antidepressants are used they should be used with caution. Antidepressants are a concern due to the possibility of inducing hypomanic switches or rapid cycling.

History

In 1883, Karl Ludwig Kahlbaum identified a disorder characterized by recurring mood cycles. The disorder contained both melancholic and manic episodes that occurred in a milder form than in bipolar disorder. This condition was coined "cyclothymia" by Kahlbaum and his student Ewald Hecker. Kahlbaum developed his theory of cyclothymia through his work with people presenting with these symptoms at the Kahlbaum Sanitarium in Goerlitz, Silesia (Germany). He was recognized as a leading hypnotherapist and psychotherapist of his day. He was a progressive in the field of mental health, believing that mental illness should not carry a stigma and that people dealing with mental health issues should be treated humanely. Kalhbaum was the first to recognize that people with cyclothymia often do not seek help for the disorder due to its milder symptoms.

Cyclothymia has been conceptualized in a variety of ways, including as a subtype of bipolar disorder, a temperament, a personality trait, and a personality disorder. There is also an argument that cyclothymia should be considered a neurodevelopmental disorder. The two defining features of the disorder, according to DSM-5, are the presence of depressive and hypomanic symptoms, not meeting the threshold for a depressive or hypomanic episode. Cyclothymia is also classified as a subtype of bipolar disorder in DSM-5, but some researchers disagree with this classification and argue that it should be primarily defined as an exaggeration of mood and emotional instability. In the past, cyclothymia has been conceptualized to include other characteristics in addition to the flux between depression and hypomania, such as mood reactivity, impulsivity, and anxiety.

Epidemiology

Cyclothymia, known today as Cyclothymic Disorder, tends to be underdiagnosed due to its low intensity. The exact rates for cyclothymia have not been widely studied. Some studies estimate that 5–8% are affected at some point in their life whereas other studies suggest a rate ranging 0.4–2.5%.

Males appear to be affected equally often, though women are more likely to receive treatment. Cyclothymia is diagnosed in around fifty percent of people with depression who are evaluated in psychiatric outpatient settings.

Etymology

Cyclothymia is derived from the Greek word κυκλοθυμία (from κῦκλος, kyklos, "circle" and θυμός, thymos, "mood, emotion"). Therefore, it means "to cycle or circle between moods or emotions".

Research

Whether subtypes of bipolar disorder, such as cyclothymia, truly represent separate disorders or are part of a unique bipolar spectrum is debated in research. Cyclothymia is typically not described in research studies or diagnosed in clinical settings, making it less recognizable and less understood by professionals. This absence of cyclothymia in research and clinical settings suggests that cyclothymia is either being diagnosed as another mood disorder or as a non-affective psychiatric disorder or not coming to scientific or clinical attention due to a lack of diagnostic clarity or because the nature of cyclothymia is still highly contested. Additionally, the current diagnostic criterion for cyclothymia emphasizes that symptoms are persistent, which suggests that they are enduring traits rather than a psychological state, thus, it has been argued that it should be diagnosed as a personality disorder. Since the symptoms tend to overlap with personality disorders, the validity and distinction between these two diagnostic categories has been debated.

Lastly, the tendency of cyclothymia to be comorbid with other mental disorders makes diagnosis difficult. These issues prevent consensus on the definition of cyclothymia and its relationship with other mental disorders among researchers and clinicians. This lack of consensus on an operational definition and symptom presentation is especially pronounced with children and adolescents because the diagnostic criteria have not been adequately adapted to take into account their developmental level.

Society and culture

Actor Stephen Fry has spoken about his experience with cyclothymia, which was depicted in the documentary Stephen Fry: The Secret Life of the Manic Depressive.

Singer Charlene Soraia has cyclothymia and wrote a song about her experiences with the disorder.

Temporal lobe epilepsy

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Temporal_lobe_epilepsy 

 

Temporal lobe epilepsy
Lobes of the brain. Temporal lobe in green
Specialty	Neurology, Psychiatry

In the field of neurology, temporal lobe epilepsy is an enduring brain disorder that causes unprovoked seizures from the temporal lobe. Temporal lobe epilepsy is the most common type of focal onset epilepsy among adults. Seizure symptoms and behavior distinguish seizures arising from the medial temporal lobe from seizures arising from the lateral (neocortical) temporal lobe. Memory and psychiatric comorbidities may occur. Diagnosis relies on electroencephalographic (EEG) and neuroimaging studies. Anticonvulsant medications, epilepsy surgery and dietary treatments may improve seizure control.

Types

Under the International League Against Epilepsy (ILAE) 2017 classification of the epilepsies, focal onset epilepsy occurs from seizures arising from a biological neural network within a single cerebral hemisphere. Temporal lobe epilepsy occurs from seizures arising within the temporal lobe. Temporal lobe epilepsy is the most common focal onset epilepsy, and 80% of temporal lobe epilepsy is mesial (medial) temporal lobe epilepsy, temporal lobe epilepsy arising from the inner (medial) part of the temporal lobe that may involve the hippocampus, parahippocampal gyrus or amygdala. The less common lateral temporal lobe or neocortical temporal lobe seizures arise from the outer (lateral) temporal lobe. The ILAE 2017 classification distinguishes focal aware from focal impaired seizures. A focal aware temporal lobe seizure occurs if a person remains aware of what occurs during the entire seizure; awareness may be retained even if impaired responsiveness occurs during the seizure. A focal impaired awareness temporal lobe seizure occurs if a person becomes unaware during any part of the seizure.

Symptoms and behavior

Medial temporal lobe epilepsy

During a temporal lobe seizure, a person may experience a seizure aura; an aura is an autonomic, cognitive, emotional or sensory experience that commonly occurs during the beginning part of a seizure. The common mesial temporal lobe seizure auras include a rising epigastric feeling, abdominal discomfort, taste (gustatory), smell (olfactory), tingling (somatosensory), fear, déjà vu, jamais vu, flushing, or rapid heart rate (tachycardia). A person may then stare blankly, appear motionless (behavioral arrest) and lose awareness. Repeated stereotyped motor behaviors (automatisms) may occur such as repeated swallowing, lip smacking, picking, fumbling, patting or vocalizations. Dystonic posture is an unnatural stiffening of one arm occuring during a seizure. A dystonic posture on one side of the body commonly indicates seizure onset from the opposite side of the brain e.g. right arm dystonic posture arising from a left temporal lobe seizure. Impaired language function (dysphasia) during or soon following a seizure is more likely to occur when seizures arise from the language dominant side of the brain.

Lateral temporal lobe epilepsy

The common auras from seizures arising from primary auditory cortex include vertigo, humming sound, ringing sound, buzzing sound, hearing a song, hearing voices or altered hearing sensation. Lateral temporal lobe seizures arising from the temporal-parietal lobe junction may cause complex visual hallucinations. In comparison to mesial temporal lobe seizures, lateral temporal lobe seizures are briefer duration seizures, occur with earlier loss of awareness, and are more likely become a focal to bilateral tonic-clonic seizure. Impaired language function (dysphasia) during or soon following a seizure is more likely to occur when seizures arise from the language dominant side of the brain.

Comorbidities

Memory

The major cognitive impairment in mesial temporal lobe epilepsy is a progressive memory impairment. This involves declarative memory impairment, including episodic memory and semantic memory, and is worse when medications fail to control seizures. Mesial temporal lobe epilepsy arising from the language dominant hemisphere impairs verbal memory, and mesial temporal lobe epilepsy arising from the language non-dominant hemisphere impairs nonverbal memory.

Psychiatric comorbidities

Psychiatric disorders are more common among those with epilepsy, and the highest prevalence occurs among those with temporal lobe epilepsy. The most common psychiatric comorbidity is major depressive disorder. Other disorders include post-traumatic stress disorder, general anxiety disorder, psychosis, obsessive-compulsive disorder, schizophrenia, bipolar disorder, substance use disorder and a ~9% prevalence of suicide.

Personality

Main article: Geschwind syndrome

Geschwind syndrome is a syndrome of altered sexuality (most often hyposexuality), religiosity, and compulsive or extensive writing and drawing occuring in persons with temporal lobe epilepsy. However, subsequent studies did not support the association of these behavioral traits with temporal lobe epilepsy. There are reports of religious behaviors occuring in persons with temporal lobe epilepsy.

Causes

Hippocampal sclerosis, brain tumor, traumatic brain injury, cerebral vascular malformation, neuronal migration disorders, infections such as encephalitis and meningitis, autoimmune disease (limbic encephalitis) and genetic disorders may cause temporal lobe epilepsy.

Risk factors

Many persons with uncontrolled temporal lobe epilepsy had childhood febrile seizures. A brief febrile seizure only slighty increases the risk for developing afebrile seizures. However, the prolonged seizure of febrile status epilepticus leads to a 9% risk for developing epilepsy. There is no clear relationship between febrile seizures and development of hippocampal sclerosis.

Mechanisms

The neural circuit of the hippocampus shows dentate gyrus (DG). subiculum (SB). entorhinal cortex (EC), CA1 sector and CA3 sector

 

Scalp electrodes are placed to record an electroencephalogram

 

Brain MRI with hippocampus identified by cross hairs.

 

Brain positron emission tomography (PET) scan

Neuronal loss

Hippocampal sclerosis occurs with severe CA1 and less severe CA3 and CA4 neuronal loss. Experimental research has shown that N-methyl-d-aspartate receptor (NMDA) receptor activation causes neuronal cell loss, and electrical stimulation-induced animal models of temporal lobe epilepsy duplicate the cell loss pattern of temporal lobe epilepsy in humans. Repetitive seizures irreversibly damage interneurons leading to persistent loss of recurrent inhibition. Damage of GABAergic interneurons lead to loss of inhibition, uncontrolled neuronal firing, leading to seizures. The secondary epileptogenesis hypothesis is that repetitive seizures lead to interneuron loss, loss of glutamatergic principal neurons, axonal sprouting, and formation of new recurrent glutamatergic excitatory circuits leading to a more severe epilepsy. Mechanisms related to neuronal loss incompletely account for temporal lobe epilepsy as temporal lobe epilepsy may occur with only minimal neuronal cell loss.

Neuron-specific type 2 K+/Cl− cotransporter (KCC2) mutation

This KCC2 mutation prevents subicular neurons from potassium and chloride ion extrusion, leading to intracellular chloride accumulation, and positive γ-Aminobutyric acid (GABA) mediated currents. Accumulated chloride efflux through GABA receptors leads to neuronal depolarization, increased neuronal excitability and ultimately seizures. Persons with this mutation have mesial temporal lobe epilepsy with hippocampal sclerosis.

Granule cell dispersion

Dentate gyrus granule cell dispersion refers to a granule cell layer that is widened, poorly demarcated, or accompanied by granule cells outside the layer (ectopic granule cells). In the normal brain, dentate granule cells block seizure spread from entorhinal cortex to the hippocampus. A hypothesis is that granule cell dispersion may disrupt the normal mossy fiber pathway connecting granule cells and CA3 pyramidal cells leading to mossy fiber sprouting and new excitatory networks capable of generating seizures. However, a study has shown that a similar pattern of granule cell dispersion may occur in persons without epilepsy.

Cortical developmental malformations

Focal cortical dysplasia is a brain malformation that may cause temporal lobe epilepsy. This malformation may cause abnormal cortical layers (dyslamination ), occur with abnormal neurons (dysmorphic neurons, balloon cells ) and may occur with a brain tumor or vascular malformation. An abnormality of the MTOR pathway leads to hyperexcitable glutamate mediated neurons leading to seizures.

Diagnosis

A surgeon performs epilepsy brain surgery

 

Vagus nerve stimulation

 

Responsive neurostimulation device

 

Surgeon implants a brain electrode for deep brain stimulation

Electroencephalogram

The temporal lobe epileptiform discharge is a pattern seen on the electroencephalgram (EEG) test; temporal lobe epileptiform discharges occur between seizures and confirm the diagnosis of temporal lobe epilepsy. Long-term video-EEG monitoring may record the behavior and EEG during a seizure. Magnetoencephalography may diagnose temporal lobe epilepsy by recording epileptiform discharges or seizure patterns arising from the magnetic fields of neural electrical currents.

Neuroimaging

Neuroimaging tests may identify the cause for seizures and the seizure focus, the brain location where seizures begin. In newly diagnosed epilepsy, magnetic resonance imaging (MRI) can detect brain lesion in up to 12 to 14% of persons with epilepsy. However, for those with chronic epilepsy, MRI can detect brain lesion in 80% of the persons with epilepsy. 3-Tesla MRI scan is advised for those with evidence of focal epilepsy such as temporal lobe epilepsy. Abnormalities identified by MRI scan include hippocampal sclerosis, focal cortical dysplasia, other cortical developmental brain malformations, developmental and low-grade tumors, cavernous hemangioma,hypoxic-ischemic brain injury, traumatic brain injury and encephalitis.

¹⁸F-fluorodeoxyglucose (¹⁸F-FDG) brain positron emission tomography (PET) may show a brain region of decreased glucose metabolism at a time between seizures; this hypometabolic region may correspond to the seizure focus, and PET scan is more sensitive for temporal lobe seizure focus localization compared to epilepsy arising from other brain lobes. Single-photon emission computed tomography (SPECT) may show a region of decreased blood flow occurring 40-60 seconds after injection during the seizure; this reduced blood flow region may correspond to the seizure focus.

Computed tomography (CT) scan is less sensitive than MRI scan for identifying small tumors, vascular malformations, cortical developmental brain malformations, and abnormalities in the medial temporal lobe. CT scan is advised in emergencies when the suspected cause of epilepsy may be intracerebral hemorrhage, brain abscess, large cerebral infarction or subdural empyema. A person who requires neuroimaging but cannot have a MRI scan due to implanted devices such as a cardiac pacemaker, defibrillator or cochlear implant may receive a CT scan. CT scan may better demonstrate calcium containing brain abnormalites causing epilepsy such as in tuberous sclerosis and Sturge–Weber syndrome.

Treatment

Medical treatment

Anticonvulsant oral medications control seizures in about two-thirds of persons with epilepsy, and control commonly occurs with one or two medications.

Surgical treatment

Those with uncontrolled seizures despite treatment with multiple anticonvulsant medications have pharmacoresistant epilepsy, and they may require epilepsy surgery to achieve seizure control.

Penfield and Flanigan first described anterior temporal lobectomy, partial surgical removal of the temporal lobe, for treatment of mesial temporal lobe epilepsy in 1950. In a prospective randomized controlled trial comparing anterior temporal lobectomy to medical therapy for pharmacoresistant temporal lobe epilepsy, surgery was more effective than medical therapy with 1-year seizure free outcome occurring in 58% of persons with anterior temporal lobectomy compared to 8% of persons with drug treatment. Among those with intractable mesial temporal lobe epilepsy and hippocampal sclerosis, about 70% become seizure-free after epilepsy surgery. Studies show that language dominant anterior temporal lobectomy may lead to verbal memory decline. However, study outcomes are more variable on language non-dominant anterior temporal lobectomy leading to nonverbal memory decline.

Magnetic resonance-guided laser interstitial thermal therapy, stereotactic radiosurgery, and stereotactic radiofrequency ablation are surgical methods that treat epilepsy by destroying the abnormal brain tissue that causes seizures.

Neurostimulation may also improve seizure control. The vagus nerve stimulator (VNS) is surgically implanted in the chest, and delivers programmed electrical stimulation to the vagus nerve in the neck. The responsive neurostimulation device is implanted in the skull, monitors electrical brain activity for seizures, and responds to seizures with programmed electrical stimulation to one or two brain areas. Programmed deep brain stimulation of the anterior thalamic nucleus may treat seizures arising from more than 2 brain areas.

Dietary treatment

The ketogenic diet and modified Atkins diet are additional temporal lobe epilepsy treatment options.

Remission

Among those who develop childhood temporal lobe epilepsy, epilepsy remits in about one-third of children. Remission was more likely among those without hippocampal sclerosis, brain tumor, or focal cortical dysplasia on MRI scan.

Apparitional experience

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Apparitional_experience

In parapsychology, an apparitional experience is an anomalous experience characterized by the apparent perception of either a living being or an inanimate object without there being any material stimulus for such a perception.

In academic discussion, the term "apparitional experience" is preferred to the term "ghost" because:

1. The term ghost implies that some element of the human being survives death and, at least under certain circumstances, can make itself perceptible to living human beings. There are other competing explanations of apparitional experiences.
2. Firsthand accounts of apparitional experiences differ in many respects from their fictional counterparts in literary or traditional ghost stories and films (see below).
3. The content of apparitional experiences includes living beings, both human and animal, and even inanimate objects.

History

Attempts to apply modern scientific or investigative standards to the study of apparitional experiences began with the work of Edmund Gurney, Frederic W. H. Myers and Frank Podmore, who were leading figures in the early years of the Society for Psychical Research (founded in 1882). Their motive, as with most of the early work of the Society, was to provide evidence for human survival after death. For this reason they had a particular interest in what are known as "crisis cases". These are cases in which a person reports having a hallucinatory experience, visual or otherwise, which apparently represents someone at a distance, this experience subsequently being considered to have coincided with that person's death, or a significant life event of some kind. If the temporal coincidence of the crisis and the distant apparitional experience cannot be explained by any conventional means, then in parapsychology the presumption is made that some as yet unknown form of communication, such as telepathy (a term coined by Myers) has taken place.

While it may be said that the work of Gurney and his colleagues failed to provide convincing evidence for either telepathy or survival of death, the large collection of firsthand written accounts which resulted from their methods may nevertheless be regarded as providing a valuable body of data concerning the phenomenology of hallucinations in the sane.

A later discussion of apparitional experiences was that of G. N. M. Tyrrell, also a leading member of the Society for Psychical Research of his day. He accepted the hallucinatory character of the experience, pointing out that it is virtually unknown for firsthand accounts to claim that apparitional figures leave any of the normal physical effects, such as footprints in snow, that one would expect of a real person. He develops the idea that the apparition may be a way for the unconscious part of the mind to bring to consciousness information that has been paranormally acquired – in crisis cases, for example. He introduces an evocative metaphor of a mental "stage-carpenter", behind the scenes in the unconscious part of the mind, and constructing the quasi-perceptual experience that eventually appears on the stage of consciousness, so that it embodies paranormal information in a symbolic way, a person drowning at a distance appearing soaked in water, for example.

The study and discussion of apparitions developed in a different direction in the 1970s, with the work of Celia Green and Charles McCreery. They were not primarily interested in the question of whether apparitions could shed any light on the existence or otherwise of telepathy, or in the survival question; instead they were concerned to analyse a large number of cases with a view to providing a taxonomy of the different types of experience, viewed simply as a type of anomalous perceptual experience or hallucination.

One of the points that was highlighted by their work was point (2) listed above, namely that "real-life" accounts of apparitional experiences differ markedly from the traditional or literary ghost story. These are some of the more notable differences, at least as indicated by their own collection of 1800 firsthand accounts:

• Subjects of apparitional experiences are by no means always frightened by the experience; indeed they may find them soothing or reassuring at times of crisis or ongoing stress in their lives.
• Spontaneous apparitional experiences tend to happen in humdrum or everyday surroundings, and under conditions of low central nervous system arousal, most often in the subject's own home – while doing housework, for example. By contrast, subjects who visit reputedly haunted locations in hopes of "seeing a ghost" are more often than not disappointed.
• Apparitions tend to be reported as appearing solid and not transparent; indeed they may be so realistic in a variety of ways as to deceive the percipient as to their hallucinatory nature; in some cases the subject only achieves insight after the experience has ended.
• It is unusual for an apparitional figure to engage in any verbal interaction with the percipient; this is consistent with the finding that the majority of such experiences only involve one sense (most commonly the visual).

Psychological implications

Psychological theories of perception

Apparitional experiences have relevance to psychological theories of perception, and in particular to the distinction between top-down and bottom-up approaches (cf. article on Top-down and bottom-up design). Top-down theories, such as that of Richard Langton Gregory, who conceives of perception as a process whereby the brain makes a series of hypotheses about the external world, stress the importance of central factors such as memory and expectation in determining the phenomenological content of perception; while the bottom-up approach, exemplified by the work of James J. Gibson, emphasises the role of the external sensory stimulus.

Apparitional experiences would seem to lend support to the importance of central factors, since they represent a form of quasi-perceptual experience in which the role of external stimuli is minimal or possibly non-existent, while the experience nevertheless continues to be phenomenologically indistinguishable from normal perception, at least in some cases.

Schizotypy

The interest of apparitional experiences to psychology has acquired an added dimension in recent years with the development of the concept of schizotypy or psychosis-proneness. This is conceived of as a dimension of personality, continuously distributed throughout the normal population, and analogous to the dimensions of extraversion or neuroticism. As long as mental illness is regarded under the disease model, according to which a person either does or does not 'have' schizophrenia or manic depression, just as a person either does or does not have syphilis or tuberculosis, then to talk of the occurrence of an apparitional or hallucinatory experience in a normal person is either an oxymoron, or to be taken as an indication of latent or incipient psychosis. If, on the contrary, a dimensional view of the matter is taken, it becomes easier to conceive of how normal people, more or less high on the putative schizotypy dimension, might be more or less prone to anomalous perceptual experiences, without their ever tipping over into psychosis.

Green and McCreery's identification of a class of what they called 'reassuring apparitions' is of particular interest in this regard, as it suggests that the experiencing of hallucinations may even have an adaptive effect in certain subjects, making them better able to cope with adverse life events. This would fit with the model of schizotypy as essentially a normal dimension of personality, and might help to explain why the proneness to anomalous perceptual experiences has apparently not been 'weeded out' by the process of natural selection.

Philosophical implications

Direct realism

Apparitional experiences also have implications for the philosophy of perception. The occurrence of hallucinations, that is, perceptual experiences 'having the character of sense perception, but without relevant or adequate sensory stimulation [...]', have long been one of the standard objections to the philosophical theory of direct realism. According to this theory we are in some sense in direct contact with the external world when we seem to be perceiving it, and not merely in direct contact with some mediating representation in our mind, such as a sense-datum or an image, which may or may not correspond to external reality. The psychologist J.J. Gibson, referred to above, became an advocate of the philosophical theory of direct realism.

Hallucinatory experiences reported by sane people do not pose any new problem in principle for the theory of direct realism, other than that posed already by the more widely discussed hallucinations reported by people in a state of psychosis or under other abnormal conditions such as sensory deprivation. They pose the problem in a particularly stark way, for the following reasons:

Scepticism about the status of verbal reports

In the case of hallucinations reported to have occurred in pathological or abnormal states there is some scope for uncertainty about the accuracy, or even the meaning, of the percipient's verbal report. Horowitz, for example, summarising his experience of questioning patients with chronic schizophrenia about their visual experiences during painting sessions, wrote:

'It was necessary to persist beyond initial verbal descriptions of their hallucinations, and insist that the patient describe and draw what he had seen. Initial descriptions of "vicious snakes" might then be drawn and redescribed as wavy lines. "Two armies struggling over my soul" arose from the subjective experience of seeing moving sets of dots. "Spiders" might be reduced, when the patient stated and drew what he actually saw, to a few radiating lines. In drawings of their hallucinations patients could often distinguish between those forms which duplicated what they saw with their eyes from those forms which were what they "made out of it".'

Such difficulties of interpretation are much less obvious in the case of written reports by ostensibly normal subjects, in good health and not medicated at the time of the experience.

Extreme realism of the experience

At least some of the apparitional experiences reported by normal subjects appear to mimic normal perception to such a degree that the subject is deceived into thinking that what they are experiencing actually is normal perception. Similar close mimicking of normal perception is reported by some of the subjects of a lucid dream and out-of-body experiences, which therefore pose similar problems for the theory of direct realism.

Representationalism

Apparitional experiences appear prima facie more compatible with the philosophical theory of representationalism. According to this theory, the immediate objects of experience when we are perceiving the world normally are representations of the world, rather than the world itself. These representations have been variously called sense-data or images. In the case of an apparitional experience one might say that the subject is aware of sense-data or images which happen not to correspond to, or represent, the external world in the normal way.

The philosophical implications of hallucinatory experiences in the sane are discussed by McCreery. He argues that they provide empirical support for the theory of representationalism rather than direct realism.