Conversion
disorder is a neurosis marked by the appearance of physical symptoms such
as partial loss of muscle function without physical cause but in the presence
of psychological conflict. Symptoms include numbness, blindness, paralysis, or
fits without a neurological
cause. It is thought that these problems arise in response to difficulties in
the patient's life, and conversion is considered a psychiatric
disorder in the Diagnostic and
Statistical Manual of Mental Disorders fourth edition (DSM-IV).
Formerly known as
"hysteria", the disorder has arguably been
known for millennia, though it came to greatest prominence at the end of the
19th century, when the neurologists Jean-Martin Charcot and Sigmund
Freud and psychiatrist Pierre Janet focused their studies on the subject. The
term "conversion" has its origins in Freud's doctrine that anxiety is
"converted" into physical symptoms.Though previously thought to
have vanished from the west in the 20th century, some research has suggested it
is as common as ever.
One or more symptoms or deficits
are present that affect voluntary motor or sensory function suggestive of
a neurologic or other general medical condition.
Psychological factors are judged,
in the clinician's belief, to be associated with the symptom or deficit
because conflicts or other stressors precede the initiation or
exacerbation of the symptom or deficit. A diagnosis where the stressor
precedes the onset of symptoms by up to 15 years is not unusual.
The symptom or deficit, after
appropriate investigation, cannot be explained fully by a general medical
condition, the direct effects of a substance, or as a culturally
sanctioned behavior or experience.
The symptom or deficit causes
clinically significant distress or impairment in social, occupational, or
other important areas of functioning or warrants medical evaluation.
The nature of the association
between the psychological factors and the neurological symptoms remains
unclear. Earlier versions of the DSM-IV employed psychodynamic
concepts, but these have been incrementally removed from successive versions.
The tenth revision
of the World Health Organization'sInternational
Classification of Diseases uses the term "conversion" as an
alternative descriptor for the dissociative disorders class of mental and
behavioural disorders (i.e. the F44 class), with the explicit suggestion that dissociative
and conversion symptoms probably share common psychological mechanisms. In
ICD-10, the dissociative [conversion] disorders class includes 10 disorders
that, in addition to specific criteria for each individual disorder, must each
meet the following general criteria:
No evidence of a physical disorder
that can explain the symptoms that characterize the disorder (but physical
disorders may be present that give rise to other symptoms);
Convincing associations in time
between the symptoms of the disorder and stressful events, problems or
needs.
History
In the 19th century,
physicians such as Silas Weir Mitchell in the US and Paul Briquet and Jean-Martin Charcot in France developed ideas
about patients sharing unexplained neurological symptoms. Charcot specialised
in treating patients who were suffering from a variety of unexplained physical
symptoms including paralysis, contractures (muscles which contract and cannot
be relaxed) and seizures. Some of these patients sporadically and compulsively
adopted a bizarre posture (christened arc-de-cercle) in which they
arched their body backwards until they were supported only by their head and
their heels.
The term
"Conversion disorder" originated with Freud. He viewed these
apparently neurological symptoms as a result of the conversion of intrapsychic
distress into physical symptoms. This distress was thought to cause the brain
to unconsciously disable or impair a bodily function as a side effect of the
original repression, which served to relieve the patient's anxiety. However,
recent evidence suggests that patients do remain distressed by their symptoms
in the long term
It has also been
suggested that at least some of the classic psychoanalytic cases of hysteria,
such as "Anna
O.", may actually have suffered from organic illness. In fact, in
Studies On Hysteria in which Breuer's Anna O. case was first presented, Freud
wrote this: "Others of the patient's symptoms were not of a hysterical
nature at all. This is true, for example, of the neck cramps, which I consider
a modified version of migraine and which as such are not to be classified as a
neurosis but as an organic disorder. Hysterical symptoms, however, regularly
become attached to these." Freud believed that all hysterical symptoms
ultimately have some organic components.
Presentation
Conversion disorder
can present with any motor or sensory symptom including any of the following:
Weakness/paralysis of a limb or the
entire body (hysterical paralysis or motor conversion disorders)
Impaired vision (hysterical
blindness) or impaired hearing
Hallucinations of a childish or
fantastical nature
Tourette-like symptoms
Mass psychogenic illness
The DSM-IV-TR
does not have specific diagnosis for mass psychogenic illness but the text
describing conversion disorder states that "In 'epidemic hysteria,' shared
symptoms develop in a circumscribed group of people following 'exposure' to a
common precipitant."
Paranoid personality disorder is a mental
disorder characterized by paranoia and a pervasive, long-standing suspiciousness and
generalized mistrust
of others. Individuals with this personality disorder may be hypersensitive,
easily feel slighted, and habitually relate to the world by vigilant scanning
of the environment for clues or suggestions that may validate their fears or
biases. Paranoid individuals are eager observers. They think they are in danger
and look for signs and threats of that danger, potentially not appreciating
other evidence. They tend to be guarded and suspicious and have quite
constricted emotional lives. Their reduced capacity for meaningful emotional involvement
and the general pattern of isolated
withdrawal often lend a quality of schizoid
isolation to their life experience. People with this particular disorder may or
may not have a tendency to bear grudges, suspiciousness, tendency to interpret
others actions as hostile, persistent tendency to self-reference, or a
tenacious sense of personal right.
Causes
A genetic contribution to paranoid traits and a
possible genetic link between this personality disorder and schizophrenia
exist. Psychosocial theories implicate projection of negative internal feelings
and parental modeling.
It is a requirement of ICD-10 that a diagnosis of
any specific personality disorder also satisfies a set of general personality disorder criteria. It is
also pointed out that for different cultures it may be necessary to develop
specific sets of criteria with regard to social norms, rules and obligations.
APA
The American Psychiatric Association's
DSM-IV-TR
has similar criteria. They require in general the presence of lasting distrust
and suspicion of others, interpreting their motives as malevolent, from an
early adult age, occurring in a range of situations. 4 of 7 specific issues
must be present, which include different types of suspicions or doubt (such as
of being exploited, or that remarks have a subtle threatening meaning), in some
cases regarding others in general or specifically friends or partners, and in
some cases referring to a response of holding grudges or reacting angrily.
Other
Various researchers and clinicians may propoose
varieties and subsets or dimensions of personality related to the official
diagnoses. Psychologist Theodore Millon has proposed five subtypes of
paranoid personality:
Borderline personality disorder: extreme "black and white" thinking, instability in
relationships, self-image, identity and behavior often leading to
self-harm and impulsivity. Borderline personality disorder is diagnosed in
three times as many females as males.
Avoidant personality disorder: social inhibition, feelings of inadequacy, extreme
sensitivity to negative evaluation and avoidance of social interaction.
Some types of personality disorder were in previous versions of the
diagnostic manuals but have been deleted. This includes two types that were in
the DSM-III-R appendix as “Proposed diagnostic categories needing further
study” without specific criteria, namely Sadistic personality disorder (a
pervasive pattern of cruel, demeaning and aggressive behavior) and Self-defeating personality disorder
(masochistic personality disorder) (characterised by behaviour consequently
undermining the person's pleasure and goals). The psychologist Theodore
Millon and others consider some relegated diagnoses to be equally valid
disorders, and may also propose other personality disorders or subtypes,
including mixtures of aspects of different categories of the officially
accepted diagnoses.
Posttraumatic stress disorder (PTSD) is a severe anxiety
disorder that can develop after exposure to any event that results in psychological trauma. This event may involve
the threat of death to oneself or to someone else, or to one's own or someone
else's physical, sexual, or psychological integrity,
overwhelming the individual's ability to cope. As an effect of psychological trauma, PTSD is less frequent
and more enduring than the more commonly seen acute stress response. Diagnostic symptoms
for PTSD include re-experiencing the original trauma(s) through flashbacks or nightmares,
avoidance of stimuli associated with the trauma, and increased arousal—such as
difficulty falling or staying asleep, anger, and hypervigilance.
Formal diagnostic criteria (both DSM-IV-TR and
ICD-10)
require that the symptoms last more than one month and cause significant
impairment in social, occupational, or other important areas of functioning.
Classification
Posttraumatic stress disorder is classified as an anxiety
disorder, characterized by aversive anxiety-related experiences, behaviors,
and physiological
responses that develop after exposure to a psychologically traumatic event
(sometimes months after). Its features persist for longer than 30 days, which
distinguishes it from the briefer acute stress disorder. These persisting
posttraumatic stress symptoms cause significant disruptions of one or more
important areas of life function. It has three sub-forms: acute, chronic, and
delayed-onset.
Causes
Psychological
trauma
PTSD is believed to be caused by experiencing any
of a wide range of events which produces intense negative feelings of
"fear, helplessness or horror" in the observer or participant.
Sources of such feelings may include (but are not limited to):
employment
in occupations exposed to war (such as soldiers) or disaster (such as emergency service workers);
getting a
diagnosis of a life-threatening illness; or
Children or adults may develop PTSD symptoms by
experiencing bullying
or mobbing.
Approximately 25% of children exposed to family violence can experience PTSD.Preliminary research suggests that child abuse may interact with
mutations in a stress-related gene to increase the risk of PTSD in adults.
Multiple studies show that parental PTSD and other
posttraumatic disturbances in parental psychological functioning can, despite a
traumatized parent's best efforts, interfere with their response to their child
as well as their child's response to trauma.Parents with
violence-related PTSD may, for example, inadvertently expose their children to
developmentally inappropriate violent media due to their need to manage their
own emotional dysregulation. Clinical findings indicate that a failure to
provide adequate treatment to children after they suffer a traumatic
experience, depending on their vulnerability and the severity of the trauma,
will ultimately lead to PTSD symptoms in adulthood.
Evolutionary
psychology
Evolutionary psychology views different
types of fears and reactions caused by fears as adaptations
that may have been useful in the ancestral environment in order to avoid or
cope with various threats. Mammals generally display several defensive behaviors roughly
dependent on how close the threat is: avoidance, vigilant immobility,
withdrawal, aggressive defense, appeasement, and finally complete frozen
immobility (the last possibly to confuse a predator's attack reflex or to
simulate a dead and contaminated body). PTSD may correspond to and be caused by
overactivation of such fear circuits. Thus, PTSD avoidance behaviors may
correspond to mammal avoidance of and withdrawal from threats. Heightened
memory of past threats may increase avoidance of similar situations in the
future as well as be a prerequisite for analyzing the past threat and develop
better defensive behaviors if the threat should reoccur. PTSD hyperarousal may
correspond to vigilant immobility and aggressive defense. Complex post-traumatic stress
disorder (and phenomena such as the Stockholm syndrome) may in part correspond to
the appeasement stage and possibly the frozen immobility stage.
There may be evolutionary explanations for
differences in resilience to traumatic events. Thus, PTSD is rare following
traumatic fire which may be explained by events such as forest fires long being
part of the evolutionary history of mammals. On the other hand, PTSD is much
more common following modern warfare, which may be explained by modern warfare
being a new development and very unlike the quick inter-group raids that are
argued to have characterized the paleolithic.
Neuroendocrinology
PTSD symptoms may result when a traumatic event
causes an over-reactive adrenaline response, which creates deep neurological
patterns in the brain. These patterns can persist long after the event that
triggered the fear, making an individual hyper-responsive to future fearful
situations.
PTSD displays biochemical
changes in the brain and body that differ from other psychiatric disorders such
as major depression. Individuals diagnosed with PTSD respond more strongly to a
dexamethasone suppression test than
individuals diagnosed with clinical depression.
In addition, most people with PTSD also show a low
secretion of cortisol
and high secretion of catecholamines in urine, with a norepinephrine/cortisol
ratio consequently higher than comparable non-diagnosed individuals. This is in
contrast to the normative fight-or-flight response, in which both catecholamine
and cortisol levels are elevated after exposure to a stressor.
Given the strong cortisol suppression to dexamethasone
in PTSD, HPA axis abnormalities are likely predicated on strong negative
feedback inhibition of cortisol, itself likely due to an increased sensitivity
of glucocorticoid receptors. Some researchers
have associated the response to stress in PTSD with long-term exposure to high
levels of norepinephrine and low levels of cortisol, a pattern
associated with improved learning in animals.
Translating this reaction to human conditions
gives a pathophysiological explanation for PTSD by a maladaptive learning
pathway to fear response through a hypersensitive, hyperreactive, and
hyperresponsive HPA axis.
Low cortisol levels may predispose individuals to PTSD:
Following war trauma, Swedish soldiers serving in Bosnia and Herzegovina with low pre-service
salivary cortisol levels had a higher risk of reacting with PTSD symptoms,
following war trauma, than soldiers with normal pre-service levels. Because
cortisol is normally important in restoring homeostasis
after the stress response, it is thought that trauma survivors with low
cortisol experience a poorly contained—that is, longer and more
distressing—response, setting the stage for PTSD.
However, there is considerable controversy within
the medical community regarding the neurobiology of PTSD. A review of existing
studies on this subject showed no clear relationship between cortisol levels
and PTSD. Only a slight majority have found a decrease in cortisol levels while
others have found no effect or even an increase.
Neuroanatomy
Regions of the brain associated with
stress and posttraumatic stress disorder
Three areas of the brain whose function may be
altered in PTSD have been identified: the prefrontal
cortex, amygdala,
and hippocampus.
Much of this research has utilised PTSD victims from the Vietnam War. For example,
a prospective study using the Vietnam Head Injury Study showed that damage to
the prefrontal cortex may actually be protective against later development of
PTSD. In a study by Gurvits et al., combat veterans of the Vietnam War
with PTSD showed a 20% reduction in the volume of their hippocampus
compared with veterans who suffered no such symptoms. This finding could not be
replicated in chronic PTSD patients traumatized at an air show plane crash in
1988 (Ramstein, Germany).
In human studies, the amygdala has been shown to
be strongly involved in the formation of emotional memories, especially
fear-related memories. Neuroimaging studies in humans have revealed both
morphological and functional aspects of PTSD.
The amygdalocentric model of PTSD proposes that it
is associated with hyperarousal of the amygdala and insufficient top-down
control by the medial prefrontal cortex and the hippocampus
particularly during extinction. This is consistent with an interpretation of
PTSD as a syndrome of deficient extinction ability. A study at the European
Neuroscience Institute-Goettingen (Germany) found that fear extinction-induced IGF2/IGFBP7 signalling
promotes the survival of 17–19-day-old newborn hippocampal neurons. This
suggests that therapeutic strategies that enhance IGF2 signalling and adult neurogenesis
might be suitable to treat diseases linked to excessive fear memory such as PTSD. Further animal
and clinical research into the amygdala and fear
conditioning may suggest additional treatments for the condition.
Genetics
There is evidence that susceptibility to PTSD is
hereditary. For twin pairs exposed to combat in Vietnam, having a monozygotic
(identical) twin with PTSD was associated with an increased risk of the co-twin
having PTSD compared to twins that were dizygotic (non-identical twins).
Recently, it has been found that several single-nucleotide polymorphisms
(SNPs) in FK506
binding protein 5 (FKBP5) interact with childhood trauma to predict
severity of adult PTSD. These findings suggest that individuals with these SNPs
who are abused as children are more susceptible to PTSD as adults.
This is particularly interesting given that FKBP5
SNPs have previously been associated with peritraumatic dissociation (that is, dissociation at the time of the trauma),
which has itself been shown to be predictive of PTSD. Furthermore, FKBP5 may be
less expressed in those with current PTSD. Another
recent study found a single SNP in a putative estrogen response element on ADCYAP1R1
(encodes pituitary adenylate cyclase-activating polypeptide type I receptor or
PAC1) to predict PTSD diagnosis and symptoms in females. Incidentally, this SNP
is also associated with fear discrimination. The study suggests that
perturbations in the PACAP-PAC1
pathway are involved in abnormal stress responses underlying PTSD.
Risk factors
Although most people (50–90%) encounter trauma
over a lifetime, only about 8% develop full PTSD. Vulnerability to PTSD
presumably stems from an interaction of biological diathesis, early childhood
developmental experiences, and trauma severity.
Predictor models have consistently found that
childhood trauma, chronic adversity, and familial stressors increase risk for
PTSD as well as risk for biological markers of risk for PTSD after a traumatic
event in adulthood. This effect of childhood trauma, which is not well
understood, may be a marker for both traumatic experiences and attachment
problems. Proximity to, duration of, and severity of the trauma also make an
impact, and interpersonal traumas cause more problems than impersonal ones.
Military
experience
Schnurr, Lunney, and Sengupta identified risk
factors for the development of PTSD in Vietnam
veterans. Among those are:
Hispanic
ethnicity, coming from an unstable family, being punished severely
during childhood, childhood asocial behavior, and depression as
pre-military factors
Recent
stressful life events, post-Vietnam
trauma, and depression as post-military factors
They also identified certain protective factors,
such as:
Japanese-American ethnicity, high school
degree or college education, older age at entry to war, higher
socioeconomic status, and a more positive paternal relationship as
pre-military protective factors
Social
support at homecoming and current social support as post-military factors.
Other research also indicates the protective effects of social support in
averting PTSD or facilitating recovery if it develops.
There may also be an attitudinal component; for
example, a soldier who believes that they will not sustain injuries may be more
likely to develop symptoms of PTSD than one who anticipates the possibility,
should either be wounded. Likewise, the later incidence of suicide among those
injured in home fires above those injured in fires in the workplace suggests
this possibility.
Foster care
In the Casey Family Northwest Alumni Study,
conducted in conjunction with researchers from the Harvard Medical School in Oregon and
Washington state, the rate of PTSD in adults who were in foster care
for one year between the ages of 14–18 was found to be higher than that of
combat veterans. Up to 25 percent of those in the study meet the diagnostic
criteria for PTSD as compared to 12–13 percent of Iraq war veterans and 15 percent of
Vietnam War veterans, and a rate of 4 percent in the general population. The
recovery rate for foster home alumni was 28.2% as opposed to 47% in the general
population.
Dubner and Motta (1999) found that 60% of children
in foster care who had experienced sexual abuse had PTSD, and 42% of those who
had been physically abused met the PTSD criteria. PTSD was also found in 18% of
the children who were not abused. These children may have developed PTSD due to
witnessing violence in the home, or as a result of real or perceived parental
abandonment.
This must have involved both (a) loss of
"physical integrity", or risk of serious injury or death, to self or
others, and (b) a response to the event that involved intense fear, horror, or
helplessness (or in children, the response must involve disorganized or
agitated behavior). (The DSM-IV-TR criterion differs substantially from the previous
DSM-III-R stressor criterion, which specified the traumatic event should be of
a type that would cause "significant symptoms of distress in almost
anyone," and that the event was "outside the range of usual human
experience.")
B: Persistent
re-experiencing
One or more of these must be present in the
victim: flashback memories, recurring
distressing dreams, subjective re-experiencing of the traumatic event(s), or
intense negative psychological or physiological response to any objective or
subjective reminder of the traumatic event(s).
C: Persistent
avoidance and emotional numbing
This involves a sufficient level of:
avoidance
of stimuli associated with the trauma, such as certain thoughts or
feelings, or talking about the event(s);
avoidance
of behaviors, places, or people that might lead to distressing memories;
inability
to recall major parts of the trauma(s), or decreased involvement in
significant life activities;
decreased
capacity (down to complete inability) to feel certain feelings;
an
expectation that one's future will be somehow constrained in ways not
normal to other people.
D: Persistent
symptoms of increased arousal not present before
These are all physiological response issues, such
as difficulty falling or staying asleep, or problems with anger, concentration,
or hypervigilance.
E: Duration of
symptoms for more than 1 month
If all other
criteria are present, but 30 days have not elapsed, the individual is diagnosed
with Acute
stress disorder.
F: Significant impairment
The symptoms reported must lead to
"clinically significant distress or impairment" of major domains of
life activity, such as social relations, occupational activities, or other
"important areas of functioning".
Dissociative identity disorder (DID) is a psychiatric diagnosis
and describes a condition in which a person displays multiple distinct identities (known as alters or parts),
each with its own pattern of perceiving and interacting with the environment.
In the International
Statistical Classification of Diseases and Related Health Problems the name
for this diagnosis is multiple personality disorder. In both systems of
terminology, the diagnosis requires that at least two personalities (one may be
the host) routinely take control of the individual's behavior with an
associated memory loss that goes beyond normal forgetfulness; in
addition, symptoms cannot be the temporary effects of drug
use or a general medical condition. DID is less common than other dissociative disorders, occurring in
approximately 1% of dissociative cases, and is often comorbid
with other disorders.
There is a great deal of controversy
surrounding the topic of DID. The validity of DID as a medical diagnosis has
been questioned, and some researchers have suggested that DID may exist
primarily as an iatrogenic adverse effect of therapy. DID is diagnosed
significantly more frequently in North America than in the rest of the world.
Signs
and symptoms
Individuals diagnosed with DID
demonstrate a variety of symptoms with wide fluctuations across time;
functioning can vary from severe impairment in daily functioning to normal or
high abilities. Symptoms can include:
Disruption of identity characterized by two
or more distinct personality states
Multiple mannerisms, attitudes and beliefs
Pseudoseizures or other conversion symptoms
Somatic symptoms that vary across identities
Distortion or loss of subjective time (a long
time)
Reviews of the literature have
discussed the findings of various psychophysiologic
investigations of DID. Many of the investigations include testing and
observation in a single person with different alters. Different alter states
have shown distinct physiological markers and some EEG studies have shown distinct differences
between alters in some subjects, while other subjects' patterns were consistent
across alters.
Neuroimaging studies of
individuals with dissociative disorders have found higher than normal levels of
memory encoding and a smaller than normal parietal
lobe.
Another study concluded that the
differences involved intensity of concentration, mood changes, degree of muscle
tension, and duration of recording, rather than some inherent difference
between the brains of people diagnosed with DID. Brain imaging studies have
corroborated the transitions of identity in some DID sufferers. A link between epilepsy and
DID has been postulated but this is disputed. Some brain
imaging studies have shown differing cerebral blood flow with different alters, and
distinct differences overall between subjects with DID and a healthy control
group.
A different imaging study showed
that findings of smaller hippocampal volumes in patients with a history of
exposure to traumatic stress and an accompanying
stress-related psychiatric disorder were also demonstrated in DID. This study
also found smaller amygdala volumes. Studies have demonstrated various changes
in visual parameters between alters. One twin study
showed heritable factors were present in DID.
Causes
This disorder is theoretically
linked with the interaction of overwhelming stress, traumatic antecedents, insufficient
childhood nurturing, and an innate ability to dissociate
memories or experiences from consciousness.
A high percentage of patients report child abuse.
People diagnosed with DID often report that they have experienced severe
physical and sexual abuse, especially during early to mid
childhood. Several psychiatric rating scales of DID sufferers suggested that
DID is strongly related to childhood trauma rather than to an underlying electrophysiological
dysfunction.
Others believe that the symptoms
of DID are created iatrogenically by therapists using certain treatment
techniques with suggestible patients, but this idea is not universally
accepted. Skeptics have suggested that a small subset of doctors are
responsible for the majority of diagnoses that a small number of therapists
were responsible for diagnosing the majority of individuals with DID.
Psychologist Nicholas Spanos and others skeptical of the
condition have suggested that in addition to iatrogenesis, DID may be the
result of role-playing rather than separate personalities, though
others disagree, pointing to a lack of incentive to manufacture or maintain separate
personalities and point to the claimed histories of abuse of these patients.
Development
theory
Severe sexual, physical, or
psychological trauma in childhood by a primary
caregiver has been proposed as an explanation for the development of DID.
In this theory, awareness, memories and feelings of a harmful action or event
caused by the caregiver is pushed into the subconscious
and dissociation becomes a coping mechanism for the individual during times of
stress. These memories and feelings are later experienced as a separate entity,
and if this happens multiple times, multiple alters are created.
Bipolar disorder or bipolar affective disorder, historically known as manic–depressive
disorder, is a psychiatric diagnosis that
describes a category of mood disorders defined by the presence of one or
more episodes of abnormally elevated energy levels, cognition,
and mood with or without one or more depressive
episodes. The elevated moods are clinically referred to as mania or, if milder, hypomania.
Individuals who experience manic episodes also commonly experience depressive episodes, or symptoms, or a mixed state in which features of both
mania and depression are present at the same time. These events are usually
separated by periods of "normal" mood; but, in some individuals, depression and
mania may rapidly alternate, which is known as rapid
cycling. Severe manic episodes can sometimes lead to such psychotic
symptoms as delusions
and hallucinations.
The disorder has been subdivided into bipolar I,
bipolar II,
cyclothymia,
and other types, based on the nature and severity of mood episodes experienced;
the range is often described as the bipolar
spectrum.
Estimates of the lifetime prevalence of bipolar disorder vary,
with studies typically giving values of the order of 1%, with higher figures
given in studies with looser definitions of the condition. The onset of full symptoms
generally occurs in late adolescence or young adulthood. Diagnosis is based on
the person's self-reported experiences, as well as observed behavior. Episodes
of abnormality are associated with distress and disruption and an elevated risk
of suicide,
especially during depressive episodes. In some cases, it can be a devastating
long-lasting disorder. In others, it has also been associated with creativity,
goal striving, and positive achievements. There is significant evidence to
suggest that many people with
creative talents have also suffered from some form of bipolar disorder. It is
often suggested that creativity and bipolar disorder are
linked.
Genetic factors
contribute substantially to the likelihood of developing bipolar disorder, and
environmental factors are also implicated. Bipolar disorder is often treated
with mood stabilizing medications and,
sometimes, other psychiatric drugs. Psychotherapy
also has a role, often when there has been some recovery of the subject's
stability. In serious cases, in which there is a risk of harm to oneself or
others, involuntary commitment may be used. These
cases generally involve severe manic episodes with dangerous behavior or
depressive episodes with suicidal
ideation. There are widespread problems with social
stigma, stereotypes, and prejudice
against individuals with a diagnosis of bipolar disorder. People with bipolar
disorder exhibiting psychotic symptoms can sometimes be misdiagnosed as having schizophrenia,
another, different, serious mental illness.
The current term bipolar
disorder is of fairly recent origin and refers to the cycling between high
and low episodes (poles). A relationship between mania and melancholia
had long been observed, although the basis of the current conceptualisation can
be traced back to French psychiatrists in the 1850s. The term
"manic-depressive illness" or psychosis was coined by German
psychiatrist Emil Kraepelin in the late nineteenth century,
originally referring to all kinds of mood disorder. German psychiatrist Karl
Leonhard split the classification again in 1957, employing the terms unipolar
disorder (major depressive disorder) and bipolar
disorder.
Signs
and symptoms
Bipolar disorder is a condition
in which people experience abnormally elevated (manic or hypomanic) and, in
many cases, abnormally depressed states for periods of time in a way that
interferes with functioning. Not everyone's symptoms are the same, and there is
no simple physiological test to confirm the disorder. Bipolar disorder can
appear to be unipolar depression. Diagnosing bipolar
disorder is often difficult, even for mental health professionals. What
distinguishes bipolar disorder from unipolar depression is that the affected
person experiences states of mania and depression. Often bipolar is
inconsistent among patients because some people feel depressed more often than
not and experience little mania whereas others experience predominantly manic
symptoms. Additionally, the younger the age of onset—bipolar disorder starts in
childhood or early adulthood in most patients—the more likely the first few
episodes are to be depression. Because a bipolar diagnosis requires a manic or
hypomanic episode, many patients are initially diagnosed and treated as having
major depression.
Depressive
episode
Signs and symptoms of the
depressive phase of bipolar disorder include persistent feelings of sadness, anxiety, guilt, anger, isolation, or hopelessness;
disturbances in sleep and appetite; fatigue and loss of interest in usually
enjoyable activities; problems concentrating; loneliness, self-loathing, apathy
or indifference; depersonalization; loss of interest in sexual
activity; shyness or social anxiety; irritability, chronic pain (with or
without a known cause); lack of motivation; and morbid suicidal ideation. In
severe cases, the individual may become psychotic, a
condition also known as severe bipolar depression with psychotic features.
These symptoms include delusions or, less commonly, hallucinations,
usually unpleasant. A major depressive episode persists for at least two weeks,
and may continue for over six months if left untreated.
Manic
episode
Mania is the signature
characteristic of bipolar disorder and, depending on its severity, is how the
disorder is classified. Mania is generally characterized by a distinct period
of an elevated mood, which can take the form of euphoria. People commonly
experience an increase in energy and a decreased need for sleep, with many
often getting as little as three or four hours of sleep per night, while others
can go days without sleeping. A person may exhibit pressured
speech, with thoughts experienced as racing. Attention span is
low, and a person in a manic state may be easily distracted. Judgment may
become impaired, and sufferers may go on spending sprees or engage in behavior
that is quite abnormal for them. They may indulge in substance abuse,
particularly alcohol or other depressants, cocaine or other stimulants, or
sleeping pills. Their behavior may become aggressive, intolerant, or intrusive.
People may feel out of control or unstoppable, or as if they have been
"chosen" and are "on a special mission" or have other
grandiose or delusional ideas. Sexual drive may increase. At more extreme
phases of bipolar I, a person in a manic state can begin to experience psychosis, or
a break with reality, where thinking is affected along with mood. Some people
in a manic state experience severe anxiety and are
very irritable (to the point of rage), while others are euphoric and grandiose.
To be diagnosed with mania
according to the Diagnostic and Statistical Manual of Mental Disorders (DSM), a
person must experience this state of elevated or irritable mood, as well as
other symptoms, for at least one week, less if hospitalization is required.
Hypomania is generally a mild to
moderate level of mania, characterized by optimism, pressure of speech and
activity, and decreased need for sleep. Generally, hypomania does not inhibit
functioning like mania. Many people with hypomania are actually in fact more
productive than usual, while manic individuals have difficulty completing tasks
due to a shortened attention span. Some people have increased creativity while
others demonstrate poor judgment and irritability. Many people experience
signature hypersexuality. These persons generally have increased
energy and tend to become more active than usual. They do not, however, have delusions or
hallucinations. Hypomania can be difficult to diagnose because it may masquerade
as mere happiness, though it carries the same risks as mania.
Hypomania may feel good to the
person who experiences it. Thus, even when family and friends learn to
recognize the mood swings, the individual often will deny that anything is
wrong. Also, the individual may not be able to recall the events that took
place while they were experiencing hypomania. What might be called a
"hypomanic event", if not accompanied by complementary depressive
episodes ("downs", etc.), is not typically deemed as problematic: The
"problem" arises when mood changes are uncontrollable and, more
importantly, volatile or "mercurial". If unaccompanied by depressive
counterpart episodes or otherwise general irritability,
this behavior is typically called hyperthymia,
or happiness,
which is, of course, perfectly normal.[citation needed] Indeed, the
most elementary definition of bipolar disorder is an often "violent"
or "jarring" state of essentially uncontrollable oscillation
between hyperthymia
and dysthymia.
If left untreated, an episode of hypomania can last anywhere from a few days to
several years. Most commonly, symptoms continue for a few weeks to a few
months.
Mixed
affective episode
In the context of bipolar
disorder, a mixed state is a condition during which symptoms of mania and clinical depression occur simultaneously.
Typical examples include tearfulness during a manic episode or racing thoughts
during a depressive episode. Individuals may also feel incredibly frustrated in
this state, since one may feel like a failure and at the same time have a flight
of ideas. Mixed states are often the most dangerous period of mood
disorders, during which substance abuse, panic
disorder, suicide
attempts, and other complications increase greatly.
Associated
features
Associated features are clinical
phenomena that often accompany the disorder but are not part of the diagnostic
criteria for the disorder. There are several childhood precursors in children
who later receive a diagnosis of bipolar disorder. They may show subtle early
traits such as mood abnormalities, full major depressive episodes, and ADHD. BD is also
accompanied by changes in cognitive processes and abilities. This include reduced attentional
and executive capabilities and impaired memory. How the
individual processes the world also depends on the phase of the disorder, with
differential characteristics between the manic, hypomanic and depressive
states. Some studies have found a significant association between bipolar
disorder and creativity.
