What is Paraphrenia?

Introduction

Paraphrenia is a mental disorder characterised by an organised system of paranoid delusions with or without hallucinations (the positive symptoms of schizophrenia) and without deterioration of intellect or personality (its negative symptom).

This disorder is also distinguished from schizophrenia by a lower hereditary occurrence, less premorbid maladjustment, and a slower rate of progression. Onset of symptoms generally occurs later in life, near the age of 60. The prevalence of the disorder among the elderly is between 0.1% and 4%.

Paraphrenia is not included in the DSM-5; psychiatrists often diagnose patients presenting with paraphrenia as having atypical psychosis, delusional disorder, psychosis not otherwise specified, schizoaffective disorders, and persistent persecutory states of older adults. Recently, mental health professionals have also been classifying paraphrenia as very late-onset schizophrenia-like psychosis.

In the Russian psychiatric manuals, paraphrenia (or paraphrenic syndrome) is the last stage of development of paranoid schizophrenia. “Systematised paraphrenia” (with systematised delusions i. e. delusions with complex logical structure) and “expansive-paranoid paraphrenia” (with expansive/grandiose delusions and persecutory delusions) are the variants of paranoid schizophrenia (F20.0). Sometimes systematised paraphrenia can be seen with delusional disorder (F22.0). The word is from Ancient Greek: παρά – beside, near + φρήν – intellect, mind.

Brief History

The term paraphrenia was originally popularised by Karl Ludwig Kahlbaum in 1863 to describe the tendency of certain psychiatric disorders to occur during certain transitional periods in life (describing paraphrenia hebetica as the insanity of the adolescence and paraphrenia senilis as the insanity of the elders.

The term was also used by Sigmund Freud for a short time starting in 1911 as an alternative to the terms schizophrenia and dementia praecox, which in his estimation did not correctly identify the underlying condition, and by Emil Kraepelin in 1912/1913, who changed its meaning to describe paraphrenia as it is understood today, as a small group of individuals that have many of the symptoms of schizophrenia with a lack of deterioration and thought disorder. Kraepelin’s study was discredited by Wilhelm Mayer in 1921 when he conducted a follow-up study using Kraepelin’s data. His study suggested that there was little to no discrimination between schizophrenia and paraphrenia; given enough time, patients presenting with paraphrenia will merge into the schizophrenic pool. However, Meyer’s data are open to various interpretations. In 1952, Roth and Morrissey conducted a large study in which they surveyed the mental hospital admissions of older patients. They characterised patients as having:

“paraphrenic delusions which… occurred in each case in the setting of a well-preserved intellect and personality, were often ‘primary’ in character, and were usually associated with the passivity failings or other volitional disturbances and hallucinations in clear consciousness pathognomonic of schizophrenia”.

In recent medicine, the term paraphrenia has been replaced by the diagnosis of “very late-onset schizophrenia-like psychosis” and has also been called “atypical psychoses, delusional disorder, psychoses not otherwise specified, schizoaffective disorders, and persistent persecutory states of older adults” by psychotherapists.[4] Current studies, however, recognize the condition as “a viable diagnostic entity that is distinct from schizophrenia, with organic factors playing a role in a significant portion of patients.”[4]

Signs and Symptoms

The main symptoms of paraphrenia are paranoid delusions and hallucinations. The delusions often involve the individual being the subject of persecution, although they can also be erotic, hypochondriacal, or grandiose in nature. The majority of hallucinations associated with paraphrenia are auditory, with 75% of patients reporting such an experience; however, visual, tactile, and olfactory hallucinations have also been reported. The paranoia and hallucinations can combine in the form of “threatening or accusatory voices coming from neighbouring houses [and] are frequently reported by the patients as disturbing and undeserved”. Patients also present with a lack of symptoms commonly found in other mental disorders similar to paraphrenia. There is no significant deterioration of intellect, personality, or habits and patients often remain clean and mostly self-sufficient. Patients also remain oriented well in time and space.

Paraphrenia is different from schizophrenia because, while both disorders result in delusions and hallucinations, individuals with schizophrenia exhibit changes and deterioration of personality whereas individuals with paraphrenia maintain a well-preserved personality and affective response.

Causes

Neurological

Paraphrenia is often associated with a physical change in the brain, such as a tumour, stroke, ventricular enlargement, or neurodegenerative process. Research that reviewed the relationship between organic brain lesions and the development of delusions suggested that “brain lesions which lead to subcortical dysfunction could produce delusions when elaborated by an intact cortex”.

Predisposing Factors

Many patients who present with paraphrenia have significant auditory or visual loss, are socially isolated with a lack of social contact, do not have a permanent home, are unmarried and without children, and have maladaptive personality traits. While these factors do not cause paraphrenia, they do make individuals more likely to develop the disorder later in life.

Diagnosis

While the diagnosis of paraphrenia is absent from recent revisions of the DSM and the ICD, many studies have recognised the condition as “a viable diagnostic entity that is distinct from schizophrenia, with organic factors playing a role in a significant portion of patients.” As such, paraphrenia is seen as being distinct from both schizophrenia and progressive dementia in old age. Ravindran (1999) developed a list of criteria for the diagnosis of paraphrenia, which agrees with much of the research done up to the time it was published.

  1. A delusional disorder of at least six months duration characterized by the following:
    1. Preoccupation with one or more semi-systematised delusions, often accompanied by auditory hallucinations.
    2. Affect notably well-preserved and appropriate. Ability to maintain rapport with others.
    3. None of:
      1. Intellectual deterioration.
      2. Visual hallucinations.
      3. Incoherence.
      4. Flat or grossly inappropriate affect.
      5. Grossly disorganised behaviour at times other than during the acute episode.
    4. Disturbance of behaviour understandable in relation to the content of the delusions and hallucinations.
    5. Only partly meets criterion A for schizophrenia. No significant organic brain disorder.

Management

Research suggests that paraphrenics respond well to antipsychotic drug therapy if doctors can successfully achieve sufficient compliance. Herbert found that Stelazine combined with Disipal was an effective treatment. It promoted the discharging of patients and kept discharged patients from being readmitted later. While behaviour therapy may help patients reduce their preoccupation with delusions, psychotherapy is not currently of primary value.

Prognosis

Individuals who develop paraphrenia have a life expectancy similar to the normal population. Recovery from the psychotic symptoms seems to be rare, and in most cases paraphrenia results in in-patient status for the remainder of the life of the patient. Patients experience a slow deterioration of cognitive functions and the disorder can lead to dementia in some cases, but this development is no greater than the normal population.

Epidemiology

Studies suggest that the prevalence of paraphrenia in the elderly population is around 2-4%.

Sex Differences

While paraphrenia can occur in both men and women, it is more common in women, even after the difference has been adjusted for life expectancies. The ratio of women with paraphrenia to men with paraphrenia is anywhere from 3:1 to 45:2.

Age

It is seen mainly in patients over the age of 60, but has been known to occur in patients in their 40s and 50s.

Personality Type and Living Situation

It is suggested that individuals who develop paraphrenia later in life have premorbid personalities, and can be described as “quarrelsome, religious, suspicious or sensitive, unsociable and cold-hearted.” Many patients were also described as being solitary, eccentric, isolated and difficult individuals; these characteristics were also long-standing rather than introduced by the disorder. Most of the traits recognised prior to the onset of paraphrenia in individuals can be grouped as either paranoid or schizoid. Patients presenting with paraphrenia were most often found to be living by themselves (either single, widowed, or divorced). There have also been reports of low marriage rate among paraphrenics and these individuals also have few or no children (possibly because of this premorbid personality).

Physical Factors

The development of paranoia and hallucinations in old age have been related to both auditory and visual impairment, and individuals with paraphrenia often present with one or both of these impairments. Hearing loss in paraphrenics is associated with early age of onset, long duration, and profound auditory loss.

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What is Folie à Deux?

Introduction

Folie à deux (‘folly of two’, or ‘madness [shared] by two’), also known as shared psychosis or shared delusional disorder (SDD), is a psychiatric syndrome in which symptoms of a delusional belief, and sometimes hallucinations, are transmitted from one individual to another.

The same syndrome shared by more than two people may be called folie à… trois (‘three’) or quatre (‘four’); and further, folie en famille (‘family madness’) or even folie à plusieurs (‘madness of several’).

The disorder was first conceptualised in 19th-century French psychiatry by Charles Lasègue and Jules Falret and is also known as Lasègue-Falret syndrome.

Recent psychiatric classifications refer to the syndrome as shared psychotic disorder (DSM-4 – 297.3) and induced delusional disorder (ICD-10 – F24), although the research literature largely uses the original name.

This disorder is not in the current DSM (DSM-5), which considers the criteria to be insufficient or inadequate. DSM-5 does not consider Shared Psychotic Disorder (Folie à Deux) as a separate entity, but rather, the physician should classify it as “Delusional Disorder” or in the “Other Specified Schizophrenia Spectrum and Other Psychotic Disorder”.

Signs and Symptoms

This syndrome is most commonly diagnosed when the two or more individuals of concern live in proximity, may be socially or physically isolated, and have little interaction with other people.

Various sub-classifications of folie à deux have been proposed to describe how the delusional belief comes to be held by more than one person:

  • Folie imposée:
    • Where a dominant person (known as the ‘primary’, ‘inducer’ or ‘principal’) initially forms a delusional belief during a psychotic episode and imposes it on another person or persons (the ‘secondary’, ‘acceptor’, or ‘associate’), with the assumption that the secondary person might not have become deluded if left to his or her own devices.
    • If the parties are admitted to hospital separately, then the delusions in the person with the induced beliefs usually resolve without the need of medication.
  • Folie simultanée:
    • Either the situation where two people considered to suffer independently from psychosis influence the content of each other’s delusions so they become identical or strikingly similar, or one in which two people “morbidly predisposed” to delusional psychosis mutually trigger symptoms in each other.

Folie à deux and its more populous derivatives are in many ways a psychiatric curiosity. The current Diagnostic and Statistical Manual of Mental Disorders states that a person cannot be diagnosed as being delusional if the belief in question is one “ordinarily accepted by other members of the person’s culture or subculture.” It is not clear at what point a belief considered to be delusional escapes from the folie à… diagnostic category and becomes legitimate because of the number of people holding it. When a large number of people may come to believe obviously false and potentially distressing things based purely on hearsay, these beliefs are not considered to be clinical delusions by the psychiatric profession, and are instead labelled as mass hysteria.

As with most psychological disorders, the extent and type of delusion varies, but the non-dominant person’s delusional symptoms usually resemble those of the inducer. Prior to therapeutic interventions, the inducer typically does not realise that they are causing harm, but instead believe they are helping the second person to become aware of vital or otherwise notable information.

Types of Delusion

Psychology Today magazine defines delusions as “fixed beliefs that do not change, even when a person is presented with conflicting evidence.” Types of delusion include:

TypeDescription
Bizarre DelusionsThose which are clearly implausible and not understood by peers within the same culture, even those with psychological disorders; for example, if one thought that all of their organs had been taken out and replaced by someone else’s while they were asleep without leaving any scar and without their waking up. It would be impossible to survive such a procedure, and even surgery involving transplantation of multiple organs would leave the person with severe pain, visible scars, etc.
Non-Bizarre DelusionsCommon among those with personality disorders and are understood by people within the same culture. For example, unsubstantiated or unverifiable claims of being followed by the FBI in unmarked cars and watched via security cameras would be classified as a non-bizarre delusion; while it would be unlikely for the average person to experience such a predicament, it is possible, and therefore understood by those around them.
Mood-Congruent DelusionsThese correspond to a person’s emotions within a given timeframe, especially during an episode of mania or depression. For example, someone with this type of delusion may believe with certainty that they will win $1 million at the casino on a specific night, despite lacking any way to see the future or influence the probability of such an event. Similarly, someone in a depressive state may feel certain that their mother will get hit by lightning the next day, again in spite of having no means of predicting or controlling future events.
Mood-Neutral DelusionsThese are unaffected by mood, and can be bizarre or non-bizarre; the formal definition provided by Mental Health Daily is “a false belief that isn’t directly related to the person’s emotional state.” An example would be a person who is convinced that somebody has switched bodies with their neighbour, the belief persisting irrespective of changes in emotional status.


Biopsychosocial Effects

As with many psychiatric disorders, shared delusional disorder can negatively impact the psychological and social aspects of a person’s wellbeing. Unresolved stress resulting from a delusional disorder will eventually contribute to or increase the risk of other negative health outcomes, such as cardiovascular disease, diabetes, obesity, immunological problems, and others. These health risks increase with the severity of the disease, especially if an affected person does not receive or comply with adequate treatment.

Persons with a delusional disorder have a significantly high risk of developing psychiatric comorbidities such as depression and anxiety. This may be attributable to a genetic pattern shared by 55% of SDD patients.

Shared delusional disorder can have a profoundly negative impact on a person’s quality of life. Persons diagnosed with a mental health disorder commonly experience social isolation, which is detrimental to psychological health. This is especially problematic with SDD, as social isolation contributes to the onset of the disorder; in particular, relapse is likely if returning to an isolated living situation, in which shared delusions can be reinstated.

Causes

While the exact causes of SDD are unknown, the main two contributors are stress and social isolation.

People who are socially isolated together tend to become dependent on those they are with, leading to an inducers influence on those around them. Additionally, people developing shared delusional disorder do not have others reminding them that their delusions are either impossible or unlikely. As a result, treatment for shared delusional disorder includes those affected be removed from the inducer.

Stress is also a factor, as it is a common factor in mental illness developing or worsening. The majority of people that develop shared delusional disorder are genetically predisposed to mental illness, but this predisposition is not enough to develop a mental disorder. However, stress can increase the risk of this disorder. When stressed, an individual’s adrenal gland releases the “stress hormone” cortisol into the body, increasing the brain’s level of dopamine; this change can be linked to the development of a mental illness, such as a shared delusional disorder.

Diagnosis

SDD is often difficult to diagnose. Usually, the person with the condition does not seek out treatment, as they do not realise that their delusion is abnormal, as it comes from someone in a dominant position who they trust. Furthermore, since their delusion comes on gradually and grows in strength over time, their doubt is slowly weakened during this time. SDD is diagnosed using the DSM-5, and according to this, the patient must meet three criteria:

  • They must have a delusion that develops in the context of a close relationship with an individual with an already established delusion.
  • The delusion must be very similar or even identical to the one already established one that the primary case has.
  • The delusion cannot be better explained by any other psychological disorder, mood disorder with psychological features, a direct result of physiological effects of substance abuse or any general medical condition.

Related phenomena

Reports have stated that a phenomenon similar to folie à deux was induced by the military incapacitating agent BZ in the late 1960s.

Prevalence

SDD is most commonly found in women with slightly above-average IQs, who are isolated from their family, and who are in relationships with a dominant person who has delusions. The majority of secondary cases (people who develop the shared delusion) also meet the criteria for Dependent Personality Disorder, which is characterised by a pervasive fear that leads them to need constant reassurance, support, and guidance. Additionally, 55% of secondary cases had a relative with a psychological disorder that included delusions and, as a result, the secondary cases are usually susceptible to mental illness.

Treatment

After a person has been diagnosed, the next step is to determine the proper course of treatment. The first step is to separate the formerly healthy person from the inducer, and see if the delusion goes away or lessens over time. If this is not enough to stop the delusions, there are two possible courses of action: Medication or therapy, which is then broken down into personal therapy and/or family therapy.

With treatment, the delusions, and therefore the disease, will eventually lessen so much so, that it will practically disappear in most cases. However, if left untreated, it can become chronic and lead to anxiety, depression, aggressive behaviour, and further social isolation. Unfortunately, there are not many statistics about the prognosis of shared delusional disorder, as it is a rare disease, and it is expected that the majority of cases go unreported; however, with treatment, the prognosis is very good.

Medication

If the separation alone is not working, antipsychotics are often prescribed for a short time to prevent the delusions. Antipsychotics are medications that reduce or relieve symptoms of psychosis such as delusions or hallucinations (seeing or hearing something that is not there). Other uses of antipsychotics include stabilising moods for people with mood swings and mood disorders (i.e. in bipolar patients), reducing anxiety in anxiety disorders, and lessening tics in people with Tourettes. Antipsychotics do not cure psychosis, but they do help reduce symptoms; when paired with therapy, the person with the condition has the best chance of recovering. While antipsychotics are powerful, and often effective, they do have side effects, such as inducing involuntary movements. They should only be taken if absolutely required, and under the supervision of a psychiatrist.

Therapy

The two most common forms of therapy for people with shared delusional disorder are personal and family therapy.

  • Personal therapy:
    • Is one-on-one counselling that focuses on building a relationship between the counsellor and the patient, and aims to create a positive environment where the patient feels that they can speak freely and truthfully.
    • This is advantageous, as the counsellor can usually get more information out of the patient to get a better idea of how to help them.
    • Additionally, if the patient trusts what the counsellor says, disproving the delusion will be easier.
  • Family therapy:
    • Is a technique in which the entire family comes into therapy together to work on their relationships, and to find ways to eliminate the delusion within the family dynamic.
    • For example, if someone’s sister is the inducer, the family will have to get involved to ensure the two stay apart, and to sort out how the family dynamic will work around that.
    • The more support a patient has, the more likely they are to recover, especially since SDD usually occurs due to social isolation.

Notable Cases

  • In May 2008, in the case of twin sisters Ursula and Sabina Eriksson, Ursula ran into the path of an oncoming articulated lorry, sustaining severe injuries.
    • Sabina then immediately duplicated her twin’s actions by stepping into the path of an oncoming car; both sisters survived the incident with severe but non-life-threatening injuries.
    • It was later claimed that Sabina Eriksson was a ‘secondary’ sufferer of folie à deux, influenced by the presence or perceived presence of her twin sister, Ursula – the ‘primary’. Sabina later told an officer at the police station, “We say in Sweden that an accident rarely comes alone. Usually at least one more follows—maybe two.”
    • However, upon her release from hospital, Sabina behaved erratically before stabbing a man to death.
  • Another case involved a married couple by the name of Margaret and Michael, both aged 34 years, who were discovered to have folie à deux when they were both found to be sharing similar persecutory delusions.
    • They believed that certain persons were entering their house, spreading dust and fluff, and “wearing down their shoes.”
    • Both had, in addition, other symptoms supporting a diagnosis of emotional contagion, which could be made independently in either case.
  • Psychiatrist Reginald Medlicott published an article about the Parker-Hulme murder case, called “Paranoia of the Exalted Type in a Setting of Folie a Deux – A Study of Two Adolescent Homicides”, arguing that the intense relationship and shared fantasy world of the two teenaged friends reinforced and exacerbated the mental illness that led to the murder: “each acted on the other as a resonator, increasing the pitch of their narcissism.”
  • In 2016, a case involving a family of five from Melbourne, Australia made headlines when they abruptly fled their home and travelled more than 1,600 km (1,000 mi) across the state of Victoria, because some of the family had become convinced someone was out to kill and rob them.
    • No such evidence was found by the police, and the symptoms of those involved resolved on their own once the family returned to their home.
  • The book Bad Blood: Secrets and Lies in a Silicon Valley Startup suggests that this ailment plagued the founder of Theranos, Elizabeth Holmes, and her boyfriend and business partner, Ramesh Balwani.
  • It was suspected a family of eleven members from Burari, India had this condition.
    • On 30 June 2018, the family died by mass suicide due to the shared belief of one of its members.
  • Psychologists H. O’Connell and P.G. Doyle believe folie à plusieurs to have been at least a partial factor in the murder of Bridget Cleary.
    • In 1895, Michael Cleary convinced several friends and relatives that his wife, Bridget Cleary, was a changeling who had been replaced by a fairy.
    • They assisted him in physically abusing her to “cast the fairies” out, before he ultimately burned her to death shortly afterwards.
  • Christine and Léa Papin were two French sisters who, as live-in maids, were convicted of murdering their employer’s wife and daughter in Le Mans, France on 02 February 1933.

In Popular Culture

  • “Folie à Deux” is the title of the nineteenth episode in the fifth season of The X-Files (1998). The episode details a story of a man who believes his boss is an insect monster, a delusion that Fox Mulder begins to share after investigation.
  • Bug (2006) is a film that depicts a couple with a shared delusion that aphids are living under their skin.
  • In Season 2, Episode 3 of Criminal Minds, “The Perfect Storm” (2006), Dr. Reid mentions that the rapists had this condition.
  • In 2008, American rock band Fall Out Boy released their fourth album, Folie à Deux.
  • The independent film Apart (2011) depicts two lovers affected and diagnosed with induced delusional disorder, trying to uncover a mysterious and tragic past they share. In a 2011 interview, director Aaron Rottinghaus stated the film was based on research from actual case studies.
  • In 2011, in CSI: Miami (Season 9, Episode 15 “Blood Lust”), it was revealed the killer couple had this condition.
  • The 2011 horror film Intruders contains characters who suffer from folie à deux.
  • In 2012, in Criminal Minds (Season 7, Episode 19 “Heathridge Manor”), it was revealed the killer family had this condition.
  • 2013’s horror game “Slender: The Arrival” centres around the shared hallucination by the main character Lauren, and her friend Kate, of the monster known as “Slender Man”.
  • In 2017, in Chance (Season 2, Episode 9 “A Madness of Two”), it was revealed the villains are having this condition.
  • The Vanished (2020) shows a couple who lost a child continuing to hold on to the delusional thought of their existence.
  • Nine Perfect Strangers (miniseries) shows a couple who lost one of their two children. The couple and the surviving child have shared hallucinations of the dead child.[36]

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What is Disruptive Mood Dysregulation Disorder?

Introduction

Disruptive mood dysregulation disorder (DMDD) is a mental disorder in children and adolescents characterised by a persistently irritable or angry mood and frequent temper outbursts that are disproportionate to the situation and significantly more severe than the typical reaction of same-aged peers.

DMDD was added to the DSM-5 as a type of depressive disorder diagnosis for youths. The symptoms of DMDD resemble those of attention deficit hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), anxiety disorders, and childhood bipolar disorder.

DMDD first appeared as a disorder in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) in 2013 and is classified as a mood disorder. Treatments include medication to manage mood symptoms as well as individual and family therapy to address emotion-regulation skills. Children with DMDD are at risk for developing depression and anxiety later in life.

Brief History

Beginning in the 1990s, some clinicians began observing children with hyperactivity, irritability, and severe temper outbursts. These symptoms greatly interfered with their lives at home, school, and with friends. Because other diagnoses, like ADHD and ODD, did not capture the severity of children’s irritability and anger, many of these children were diagnosed with bipolar disorder. Longitudinal studies showed that children with chronic irritability and temper outbursts often developed later problems with anxiety and depression, and rarely developed bipolar disorder in adolescence or adulthood. Consequently, the developers of DSM-5 created a new diagnostic label, DMDD, to describe children with persistent irritability and angry outbursts. In 2013, the American Psychiatric Association (APA) added DMDD to the DSM-5 and classified it as a depressive disorder.

Signs and Symptoms

Children with DMDD show severe and recurrent temper outbursts three or more times per week. These outbursts can be verbal or behavioural. Verbal outbursts often are described by observers as “rages”, “fits”, or “tantrums”. Children may scream, yell, and cry for excessively long periods of time, sometimes with little provocation. Physical outbursts may be directed toward people or property. Children may throw objects; hit, slap, or bite others; destroy toys or furniture; or otherwise act in a harmful or destructive manner.

Children with DMDD also display persistently irritable or angry mood that is observable by others. Parents, teachers, and classmates describe these children as habitually angry, touchy, grouchy, or easily “set off”. Unlike the irritability that can be a symptom of other childhood disorders, such as ODD, anxiety disorders, and major depressive disorder (MDD), the irritability displayed by children with DMDD is not episodic or situation-dependent. In DMDD, the irritability or anger is severe and is shown most of the day, nearly every day in multiple settings, lasting for one or more years.

The DSM-5 includes several additional diagnostic criteria which describe the duration, setting, and onset of the disorder: the outbursts must be present for at least 12 months and occur in at least two settings (e.g. home and school), and it must be severe in at least one setting. Symptoms appear before the age of 10, and diagnosis must be made between ages 6 and 18.

Comorbidity

The core features of DMDD – temper outbursts and chronic irritability – are sometimes seen in children and adolescents with other psychiatric conditions. Differentiating DMDD from these other conditions can be difficult. Three disorders that most closely resemble DMDD are ADHD, oppositional defiant disorder (ODD), and bipolar disorder in children.

ADHD

ADHD is a neurodevelopmental disorder characterised by problems with inattention and/or hyperactivity-impulsivity.

ODD

ODD is a disruptive behaviour disorder characterised by oppositional, defiant, and sometimes hostile actions directed towards others.

Bipolar Disorder

One of the main differences between DMDD and bipolar disorder is that the irritability and anger outbursts associated with DMDD are not episodic; symptoms of DMDD are chronic and displayed constantly on an almost daily basis. On the other hand, bipolar disorder is characterised by distinct manic or hypomanic episodes usually lasting a few days, or a few weeks at most, that parents should be able to differentiate from their child’s typical mood and behaviour in between episodes. The DSM precludes a dual diagnosis of DMDD and bipolar disorder. Bipolar disorder alone should be used for youths who show classic symptoms of episodic mania or hypomania.

Prior to adolescence, DMDD is much more common than bipolar disorder. Most children with DMDD see a decrease in symptoms as they enter adulthood, whereas individuals with bipolar disorder typically display symptoms for the first time as teenagers and young adults. Children with DMDD are more at risk for developing MDD or generalised anxiety disorder when they are older rather than bipolar disorder.

Causes

Youth with DMDD have difficulty attending, processing, and responding to negative emotional stimuli and social experiences in their everyday lives. For example, some studies have shown youths with DMDD to have problems interpreting the social cues and emotional expressions of others. These youths may be especially bad at judging others’ negative emotional displays, such as feelings of sadness, fearfulness, and anger. Functional MRI studies suggest that under-activity of the amygdala, the brain area that plays a role in the interpretation and expression of emotions and novel stimuli, is associated with these deficits. Deficits in interpreting social cues may predispose children to instances of anger and aggression in social settings with little provocation. For examples, youths with DMDD may selectively attend to negative social cues (e.g. others scowling, teasing) and minimize all other information about the social events. They may also misinterpret the emotional displays of others, believing others’ benign actions to be hostile or threatening. Consequently, they may be more likely than their peers to act in impulsive and angry ways.

Children with DMDD may also have difficulty regulating negative emotions once they are elicited. To study these problems with emotion regulation, researchers asked children with DMDD to play computer games that are rigged so that children will lose. While playing these games, children with DMDD report more agitation and negative emotional arousal than their typically-developing peers. Furthermore, youths with DMDD showed markedly greater activity in the medial frontal gyrus and anterior cingulate cortex compared to other youths. These brain regions are important because they are involved in evaluating and processing negative emotions, monitoring one’s own emotional state, and selecting an effective response when upset, angry, or frustrated. Altogether, these findings suggest that youths with DMDD are more strongly influenced by negative events than other youths. They may become more upset and select less effective and socially acceptable ways to deal with negative emotions when they arise.

Treatment

Medication

Evidence for treatment is weak, and treatment is determined based on the physician’s response to the symptoms that people with DMDD present. Because the mood stabilizing medication, lithium, is effective in treating adults with bipolar disorder, some physicians have used it to treat DMDD although it has not been shown to be better than placebo in alleviating the signs and symptoms of DMDD.[7] DMDD is treated with a combination of medications that target the child’s symptom presentation. For youths with DMDD alone, antidepressant medication is sometimes used to treat underlying problems with irritability or sadness. For youths with unusually strong temper outbursts, an atypical antipsychotic medication, such as risperidone, may be warranted. Both medications, however, are associated with significant side effects in children. Finally, for children with both DMDD and ADHD, stimulant medication is sometimes used to reduce symptoms of impulsivity.

Psychosocial

Several cognitive-behavioural interventions have been developed to help youths with chronic irritability and temper outbursts. Because many youths with DMDD show problems with ADHD and oppositional-defiant behaviour, experts initially tried to treat these children using contingency management. This type of intervention involves teaching parents to reinforce children’s appropriate behaviour and extinguish (usually through systematic ignoring or time out) inappropriate behaviour. Although contingency management can be helpful for ADHD and ODD symptoms, it does not seem to reduce the most salient features of DMDD, namely, irritability and anger.

Epidemiology

There are not good estimates of the prevalence of DMDD, but primary studies have found a rate of 0.8 to 3.3%. Epidemiological studies show that approximately 3.2% of children in the community have chronic problems with irritability and temper, the essential features of DMDD. These problems are probably more common among clinic-referred youths. Parents report that approximately 30% of children hospitalised for psychiatric problems meet diagnostic criteria for DMDD; 15% meet criteria based on the observations of hospital staff.

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What is Combat Stress Reaction?

Introduction

Combat stress reaction (CSR) is a term used within the military to describe acute behavioural disorganisation as a direct result of the trauma of war.

Also known as “combat fatigue”, “battle fatigue”, or “battle neurosis”, it has some overlap with the diagnosis of acute stress reaction used in civilian psychiatry. It is historically linked to shell shock and can sometimes precede post-traumatic stress disorder (PTSD).

Combat stress reaction is an acute reaction that includes a range of behaviours resulting from the stress of battle that decrease the combatant’s fighting efficiency. The most common symptoms are fatigue, slower reaction times, indecision, disconnection from one’s surroundings, and the inability to prioritise. Combat stress reaction is generally short-term and should not be confused with acute stress disorder, PTSD, or other long-term disorders attributable to combat stress, although any of these may commence as a combat stress reaction. The US Army uses the term/acronym COSR (Combat Stress Reaction) in official medical reports. This term can be applied to any stress reaction in the military unit environment. Many reactions look like symptoms of mental illness (such as panic, extreme anxiety, depression, and hallucinations), but they are only transient reactions to the traumatic stress of combat and the cumulative stresses of military operations.

In World War I, shell shock was considered a psychiatric illness resulting from injury to the nerves during combat. The horrors of trench warfare meant that about 10% of the fighting soldiers were killed (compared to 4.5% during World War II) and the total proportion of troops who became casualties (killed or wounded) was about 57%. Whether a shell-shock sufferer was considered “wounded” or “sick” depended on the circumstances. When faced with the phenomenon of a minority of soldiers mentally breaking down, there was an expectation that the root of this problem lay in character of the individual soldier, not because of what they experienced on the front lines during the war. The large proportion of World War I veterans in the European population meant that the symptoms were common to the culture.

Refer to Acute Stress Disorder.

Signs and Symptoms

Combat stress reaction symptoms align with the symptoms also found in psychological trauma, which is closely related to PTSD. CSR differs from PTSD (among other things) in that a PTSD diagnosis requires a duration of symptoms over one month, which CSR does not.

Fatigue-Related Symptoms

The most common stress reactions include:

  • The slowing of reaction time.
  • Slowness of thought.
  • Difficulty prioritising tasks.
  • Difficulty initiating routine tasks.
  • Preoccupation with minor issues and familiar tasks.
  • Indecision and lack of concentration.
  • Loss of initiative with fatigue.
  • Exhaustion.

Autonomic Nervous System – Autonomic Arousal

  • Headaches.
  • Back pains.
  • Inability to relax.
  • Shaking and tremors.
  • Sweating.
  • Nausea and vomiting.
  • Loss of appetite.
  • Abdominal distress.
  • Frequency of urination.
  • Urinary incontinence.
  • Heart palpitations.
  • Hyperventilation.
  • Dizziness.
  • Insomnia.
  • Nightmares.
  • Restless sleep.
  • Excessive sleep.
  • Excessive startle.
  • Hypervigilance.
  • Heightened sense of threat.
  • Anxiety.
  • Irritability.
  • Depression.
  • Substance abuse.
  • Loss of adaptability.
  • Attempted suicides.
  • Disruptive behaviour.
  • Mistrust of others.
  • Confusion.
  • Extreme feeling of losing control.

Battle Casualty Rates

The ratio of stress casualties to battle casualties varies with the intensity of the fighting. With intense fighting, it can be as high as 1:1. In low-level conflicts, it can drop to 1:10 (or less). Modern warfare embodies the principles of continuous operations with an expectation of higher combat stress casualties.

The World War II European Army rate of stress casualties of 1 in 10 (101:1,000) troops per annum is skewed downward from both its norm and peak by data by low rates during the last years of the war.

Diagnosis

The following PIE principles were in place for the “not yet diagnosed nervous” (NYDN) cases:

  • Proximity: Treat the casualties close to the front and within sound of the fighting.
  • Immediacy: Treat them without delay and not wait until the wounded were all dealt with.
  • Expectancy: Ensure that everyone had the expectation of their return to the front after a rest and replenishment.

United States medical officer Thomas W. Salmon is often quoted as the originator of these PIE principles. However, his real strength came from going to Europe and learning from the Allies and then instituting the lessons. By the end of the war, Salmon had set up a complete system of units and procedures that was then the “world’s best practice”. After the war, he maintained his efforts in educating society and the military. He was awarded the Distinguished Service Medal for his contributions.

Effectiveness of the PIE approach has not been confirmed by studies of CSR, and there is some evidence that it is not effective in preventing PTSD.

US services now use the more recently developed BICEPS principles:

  • Brevity.
  • Immediacy.
  • Centrality or contact.
  • Expectancy.
  • Proximity.
  • Simplicity.

Between the Wars

The British government produced a Report of the War Office Committee of Inquiry into “Shell-Shock”, which was published in 1922. Recommendations from this included:

AreaDescription
In Forward AreasNo soldier should be allowed to think that loss of nervous or mental control provides an honourable avenue of escape from the battlefield, and every endeavour should be made to prevent slight cases leaving the battalion or divisional area, where treatment should be confined to provision of rest and comfort for those who need it and to heartening them for return to the front line.
In Neurological CentresWhen cases are sufficiently severe to necessitate more scientific and elaborate treatment they should be sent to special Neurological Centres as near the front as possible, to be under the care of an expert in nervous disorders. No such case should, however, be so labelled on evacuation as to fix the idea of nervous breakdown in the patient’s mind.
In Base HospitalsWhen evacuation to the base hospital is necessary, cases should be treated in a separate hospital or separate sections of a hospital, and not with the ordinary sick and wounded patients. Only in exceptional circumstances should cases be sent to the United Kingdom, as, for instance, men likely to be unfit for further service of any kind with the forces in the field. This policy should be widely known throughout the Force.
Forms of TreatmentThe establishment of an atmosphere of cure is the basis of all successful treatment, the personality of the physician is, therefore, of the greatest importance. While recognising that each individual case of war neurosis must be treated on its merits, the Committee are of opinion that good results will be obtained in the majority by the simplest forms of psycho-therapy, i.e. explanation, persuasion and suggestion, aided by such physical methods as baths, electricity and massage. Rest of mind and body is essential in all cases.
The committee are of opinion that the production of deep hypnotic sleep, while beneficial as a means of conveying suggestions or eliciting forgotten experiences are useful in selected cases, but in the majority they are unnecessary and may even aggravate the symptoms for a time.
They do not recommend psycho-analysis in the Freudian sense.
In the state of convalescence, re-education and suitable occupation of an interesting nature are of great importance. If the patient is unfit for further military service, it is considered that every endeavour should be made to obtain for him suitable employment on his return to active life.
Return to the Fighting LineSoldiers should not be returned to the fighting line under the following conditions:-
(1) If the symptoms of neurosis are of such a character that the soldier cannot be treated overseas with a view to subsequent useful employment.
(2) If the breakdown is of such severity as to necessitate a long period of rest and treatment in the United Kingdom.
(3) If the disability is anxiety neurosis of a severe type.
(4) If the disability is a mental breakdown or psychosis requiring treatment in a mental hospital.
It is, however, considered that many of such cases could, after recovery, be usefully employed in some form of auxiliary military duty.

Part of the concern was that many British veterans were receiving pensions and had long-term disabilities.

By 1939, some 120,000 British ex-servicemen had received final awards for primary psychiatric disability or were still drawing pensions – about 15% of all pensioned disabilities – and another 44,000 or so were getting pensions for ‘soldier’s heart’ or Effort Syndrome. There is, though, much that statistics do not show, because in terms of psychiatric effects, pensioners were just the tip of a huge iceberg.”

War correspondent Philip Gibbs wrote:

Something was wrong. They put on civilian clothes again and looked to their mothers and wives very much like the young men who had gone to business in the peaceful days before August 1914. But they had not come back the same men. Something had altered in them. They were subject to sudden moods, and queer tempers, fits of profound depression alternating with a restless desire for pleasure. Many were easily moved to passion where they lost control of themselves, many were bitter in their speech, violent in opinion, frightening.

One British writer between the wars wrote:

There should be no excuse given for the establishment of a belief that a functional nervous disability constitutes a right to compensation. This is hard saying. It may seem cruel that those whose sufferings are real, whose illness has been brought on by enemy action and very likely in the course of patriotic service, should be treated with such apparent callousness. But there can be no doubt that in an overwhelming proportion of cases, these patients succumb to ‘shock’ because they get something out of it. To give them this reward is not ultimately a benefit to them because it encourages the weaker tendencies in their character. The nation cannot call on its citizens for courage and sacrifice and, at the same time, state by implication that an unconscious cowardice or an unconscious dishonesty will be rewarded.

World War II

American

At the outbreak of World War II, most in the United States military had forgotten the treatment lessons of World War I. Screening of applicants was initially rigorous, but experience eventually showed it to lack great predictive power.

The US entered the war in December 1941. Only in November 1943 was a psychiatrist added to the table of organisation of each division, and this policy was not implemented in the Mediterranean Theatre of Operations until March 1944. By 1943, the US Army was using the term “exhaustion” as the initial diagnosis of psychiatric cases, and the general principles of military psychiatry were being used. General Patton’s slapping incident was in part the spur to institute forward treatment for the Italian invasion of September 1943. The importance of unit cohesion and membership of a group as a protective factor emerged.

John Appel found that the average American infantryman in Italy was “worn out” in 200 to 240 days and concluded that the American soldier “fights for his buddies or because his self respect won’t let him quit”. After several months in combat, the soldier lacked reasons to continue to fight because he had proven his bravery in battle and was no longer with most of the fellow soldiers he trained with. Appel helped implement a 180-day limit for soldiers in active combat and suggested that the war be made more meaningful, emphasizing their enemies’ plans to conquer the United States, encouraging soldiers to fight to prevent what they had seen happen in other countries happen to their families. Other psychiatrists believed that letters from home discouraged soldiers by increasing nostalgia and needlessly mentioning problems soldiers could not solve. William Menninger said after the war, “It might have been wise to have had a nation-wide educational course in letter writing to soldiers”, and Edward Strecker criticised “moms” (as opposed to mothers) who, after failing to “wean” their sons, damaged morale through letters.

Airmen flew far more often in the Southwest Pacific than in Europe, and although rest time in Australia was scheduled, there was no fixed number of missions that would produce transfer out of combat, as was the case in Europe. Coupled with the monotonous, hot, sickly environment, the result was bad morale that jaded veterans quickly passed along to newcomers. After a few months, epidemics of combat fatigue would drastically reduce the efficiency of units. Flight surgeons reported that the men who had been at jungle airfields longest were in bad shape:

Many have chronic dysentery or other disease, and almost all show chronic fatigue states. . . .They appear listless, unkempt, careless, and apathetic with almost mask-like facial expression. Speech is slow, thought content is poor, they complain of chronic headaches, insomnia, memory defect, feel forgotten, worry about themselves, are afraid of new assignments, have no sense of responsibility, and are hopeless about the future.

British

Unlike the Americans, the British leaders firmly held the lessons of World War I. It was estimated that aerial bombardment would kill up to 35,000 a day, but the Blitz killed only 40,000 in total. The expected torrent of civilian mental breakdown did not occur. The Government turned to World War I doctors for advice on those who did have problems. The PIE principles were generally used. However, in the British Army, since most of the World War I doctors were too old for the job, young, analytically trained psychiatrists were employed. Army doctors “appeared to have no conception of breakdown in war and its treatment, though many of them had served in the 1914–1918 war.” The first Middle East Force psychiatric hospital was set up in 1942. With D-Day for the first month there was a policy of holding casualties for only 48 hours before they were sent back over the Channel. This went firmly against the expectancy principle of PIE.

Appel believed that British soldiers were able to continue to fight almost twice as long as their American counterparts because the British had better rotation schedules and because they, unlike the Americans, “fight for survival” – for the British soldiers, the threat from the Axis powers was much more real, given Britain’s proximity to mainland Europe, and the fact that Germany was concurrently conducting air raids and bombarding British industrial cities. Like the Americans, British doctors believed that letters from home often needlessly damaged soldiers’ morale.

Canadian

The Canadian Army recognised combat stress reaction as “Battle Exhaustion” during the Second World War and classified it as a separate type of combat wound. Historian Terry Copp has written extensively on the subject. In Normandy, “The infantry units engaged in the battle also experienced a rapid rise in the number of battle exhaustion cases with several hundred men evacuated due to the stress of combat. Regimental Medical Officers were learning that neither elaborate selection methods nor extensive training could prevent a considerable number of combat soldiers from breaking down.”

Germans

In his history of the pre-Nazi Freikorps paramilitary organisations, Vanguard of Nazism, historian Robert G.L. Waite describes some of the emotional effects of World War I on German troops, and refers to a phrase he attributes to Göring: men who could not become “de-brutalized”.

In an interview, Dr Rudolf Brickenstein stated that:

… he believed that there were no important problems due to stress breakdown since it was prevented by the high quality of leadership. But, he added, that if a soldier did break down and could not continue fighting, it was a leadership problem, not one for medical personnel or psychiatrists. Breakdown (he said) usually took the form of unwillingness to fight or cowardice.

However, as World War II progressed there was a profound rise in stress casualties from 1% of hospitalizations in 1935 to 6% in 1942. Another German psychiatrist reported after the war that during the last two years, about a third of all hospitalisations at Ensen were due to war neurosis. It is probable that there was both less of a true problem and less perception of a problem.

Finns

The Finnish attitudes to “war neurosis” were especially tough. Psychiatrist Harry Federley, who was the head of the Military Medicine, considered shell shock as a sign of weak character and lack of moral fibre. His treatment for war neurosis was simple: the patients were to be bullied and harassed until they returned to front line service.

Earlier, during the Winter War, several Finnish machine gun operators on the Karelian Isthmus theatre became mentally unstable after repelling several unsuccessful Soviet human wave assaults on fortified Finnish positions.

Post-World War II Developments

Simplicity was added to the PIE principles by the Israelis: in their view, treatment should be brief, supportive, and could be provided by those without sophisticated training.

Peacekeeping Stresses

Peacekeeping provides its own stresses because its emphasis on rules of engagement contains the roles for which soldiers are trained. Causes include witnessing or experiencing the following:

  • Constant tension and threat of conflict.
  • Threat of land mines and booby traps.
  • Close contact with severely injured and dead people.
  • Deliberate maltreatment and atrocities, possibly involving civilians.
  • Cultural issues, e.g. male dominant attitudes towards women in different cultures.
  • Separation and home issues.
  • Risk of disease including HIV.
  • Threat of exposure to toxic agents.
  • Mission problems.
  • Return to service.

Pathophysiology

SNS Activation

Many of the symptoms initially experienced by CSR sufferers are effects of an extended activation of the human body’s fight-or-flight response. The fight-or-flight response involves a general sympathetic nervous system discharge in reaction to a perceived stressor and prepares the body to fight or run from the threat causing the stress. Catecholamine hormones, such as adrenaline or noradrenaline, facilitate immediate physical reactions associated with a preparation for violent muscular action. Although the flight-or-fight-response normally ends with the removal of the threat, the constant mortal danger in combat zones likewise constantly and acutely stresses soldiers.

General Adaptation Syndrome

The process whereby the human body responds to extended stress is known as general adaptation syndrome (GAS). After the initial fight-or-flight response, the body becomes more resistant to stress in an attempt to dampen the sympathetic nervous response and return to homeostasis. During this period of resistance, physical and mental symptoms of CSR may be drastically reduced as the body attempts to cope with the stress. Long combat involvement, however, may keep the body from homeostasis and thereby deplete its resources and render it unable to normally function, sending it into the third stage of GAS: exhaustion. Sympathetic nervous activation remains in the exhaustion phase and reactions to stress are markedly sensitised as fight-or-flight symptoms return. If the body remains in a state of stress, then such more severe symptoms of CSR as cardiovascular and digestive involvement may present themselves. Extended exhaustion can permanently damage the body.

Treatment

7 Rs

The British Army treated Operational Stress Reaction according to the 7 R’s:

  • Recognition: Identify that the individual is suffering from an Operational Stress Reaction.
  • Respite: Provide a short period of relief from the front line.
  • Rest: Allow rest and recovery.
  • Recall: Give the individual the chance to recall and discuss the experiences that have led to the reaction.
  • Reassurance: Inform the sufferer that their reaction is normal and they will recover.
  • Rehabilitation: Improve the physical and mental health of the patient until they no longer show symptoms.
  • Return: Allow the soldier to return to their unit.

BICEPS

Modern front-line combat stress treatment techniques are designed to mimic the historically used PIE techniques with some modification. BICEPS is the current treatment route employed by the US military and stresses differential treatment by the severity of CSR symptoms present in the service member. BICEPS is employed as a means to treat CSR symptoms and return soldiers quickly to combat.

The following BICEPS program is taken from the USMC combat stress handbook:

Brevity

Critical Event Debriefing should take 2 to 3 hours. Initial rest and replenishment at medical CSC (Combat Stress Control) facilities should last no more than 3 or 4 days. Those requiring further treatment are moved to the next level of care. Since many require no further treatment, military commanders expect their service members to return to duty rapidly.

Immediacy

CSC should be done as soon as possible when operations permit. Intervention is provided as soon as symptoms appear.

Centrality/Contact

Service members requiring observation or care beyond the unit level are evacuated to facilities in close proximity to, but separate from the medical or surgical patients at the BAS, surgical support company in a central location (Marines) or forward support/division support or area support medical companies (Army) nearest the service members’ unit. It is best to send Service members who cannot continue their mission and require more extensive respite to a central facility other than a hospital, unless no other alternative is possible. The Service member must be encouraged to continue to think of himself as a war fighter, rather than a patient or a sick person. The chain of command remains directly involved in the Service member’s recovery and return to duty. The CSC team coordinates with the unit’s leaders to learn whether the over-stressed individual was a good performer prior to the combat stress reaction, or whether he was always a marginal or problem performer whom the team would rather see replaced than returned. Whenever possible, representatives of the unit, or messages from the unit, tell the casualty that he is needed and wanted back. The CSC team coordinates with the unit leaders, through unit medical personnel or chaplains, any special advice on how to assure quick reintegration when the Service member returns to his unit.

Expectancy

The individual is explicitly told that he is reacting normally to extreme stress and is expected to recover and return to full duty in a few hours or days. A military leader is extremely effective in this area of treatment. Of all the things said to a Service member suffering from combat stress, the words of his small-unit leader have the greatest impact due to the positive bonding process that occurs during combat. Simple statements from the small-unit leader to the Service member that he is reacting normally to combat stress and is expected back soon have positive impact. Small-unit leaders should tell Service members that their comrades need and expect them to return. When they do return, the unit treats them as every other Service member and expects them to perform well. Service members suffering and recovering from combat stress disorder are no more likely to become overloaded again than are those who have not yet been overloaded. In fact, they are less likely to become overloaded than inexperienced replacements.

Proximity

In mobile war requiring rapid and frequent movement, treatment of many combat stress cases takes place at various battalion or regimental headquarters or logistical units, on light duty, rather than in medical units, whenever possible. This is a key factor and another area where the small-unit leader helps in the treatment. CSC and follow-up care for combat stress casualties are held as close as possible to and maintain close association with the member’s unit, and are an integral part of the entire healing process. A visit from a member of the individual’s unit during restoration is very effective in keeping a bond with the organization. A Service member suffering from combat stress reaction is having a crisis, and there are two basic elements to that crisis working in opposite directions. On the one hand, the Service member is driven by a strong desire to seek safety and to get out of an intolerable environment. On the other hand, the Service member does not want to let his comrades down. He wants to return to his unit. If a Service member starts to lose contact with his unit when he enters treatment, the impulse to get out of the war and return to safety takes over. He feels that he has failed his comrades and they have already rejected him as unworthy. The potential is for the Service member to become more and more emotionally invested in keeping his symptoms so he can stay in a safe environment. Much of this is done outside the Service member’s conscious awareness, but the result is the same. The more out of touch the Service member is with his unit, the less likely he will recover. He is more likely to develop a chronic psychiatric illness and get evacuated from the war. This is one of the essential principles of CSC.

Simplicity

Treatment is kept very simple. CSC is not therapy. Psychotherapy is not done. The goal is to rapidly restore the Service member’s coping skills so that he functions and returns to duty again. Sleep, food, water, hygiene, encouragement, work details, and confidence-restoring talk are often all that is needed to restore a Service member to full operational readiness. This can be done in units in reserve positions, logistical units or at medical companies. Every effort is made to reinforce Service members’ identity. They are required to wear their uniforms and to keep their helmets, equipment, chemical protective gear, and flak jackets with them. When possible, they are allowed to keep their weapons after the weapons have been cleared. They may serve on guard duty or as members of a standby quick reaction force.

Pre-Deployment Preparation

Screening

Historically, screening programs that have attempted to preclude soldiers exhibiting personality traits thought to predispose them to CSR have been a total failure. Part of this failure stems from the inability to base CSR morbidity on one or two personality traits. Full psychological work-ups are expensive and inconclusive, while pen and paper tests are ineffective and easily faked. In addition, studies conducted following WWII screening programs showed that psychological disorders present during military training did not accurately predict stress disorders during combat.

Cohesion

While it is difficult to measure the effectiveness of such a subjective term, soldiers who reported in a WWII study that they had a “higher than average” sense of camaraderie and pride in their unit were more likely to report themselves ready for combat and less likely to fall victim to CSR or other stress disorders. Soldiers with a “lower than average” sense of cohesion with their unit were more susceptible to stress illness.

Training

Stress exposure training or SET is a common component of most modern military training. There are three steps to an effective stress exposure programme.

StepDescription
Providing Knowledge of the Stress EnvironmentSoldiers with a knowledge of both the emotional and physical signs and symptoms of CSR are much less likely to have a critical event that reduces them below fighting capability. Instrumental information, such as breathing exercises that can reduce stress and suggestions not to look at the faces of enemy dead, is also effective at reducing the chance of a breakdown.
Skills AcquisitionCognitive control strategies can be taught to soldiers to help them recognise stressful and situationally detrimental thoughts and repress those thoughts in combat situations. Such skills have been shown to reduce anxiety and improve task performance.
Confidence Building through Application and PracticeSoldiers who feel confident in their own abilities and those of their squad are far less likely to suffer from combat stress reaction. Training in stressful conditions that mimic those of an actual combat situation builds confidence in the abilities of themselves and the squad. As this training can actually induce some of the stress symptoms it seeks to prevent, stress levels should be increased incrementally as to allow the soldiers time to adapt.

Prognosis

Figures from the 1982 Lebanon war showed that with proximal treatment, 90% of CSR casualties returned to their unit, usually within 72 hours. With rearward treatment, only 40% returned to their unit. It was also found that treatment efficacy went up with the application of a variety of front line treatment principles versus just one treatment. In Korea, similar statistics were seen, with 85% of US battle fatigue casualties returned to duty within three days and 10% returned to limited duties after several weeks.

Though these numbers seem to promote the claims that proximal PIE or BICEPS treatment is generally effective at reducing the effects of combat stress reaction, other data suggests that long term PTSD effects may result from the hasty return of affected individuals to combat. Both PIE and BICEPS are meant to return as many soldiers as possible to combat, and may actually have adverse effects on the long term health of service members who are rapidly returned to the front-line after combat stress control treatment. Although the PIE principles were used extensively in the Vietnam War, the post traumatic stress disorder lifetime rate for Vietnam veterans was 30% in a 1989 US study and 21% in a 1996 Australian study. In a study of Israeli Veterans of the 1973 Yom Kippur War, 37% of veterans diagnosed with CSR during combat were later diagnosed with PTSD, compared with 14% of control veterans.

Controversy

There is significant controversy with the PIE and BICEPS principles. Throughout a number of wars, but notably during the Vietnam War, there has been a conflict among doctors about sending distressed soldiers back to combat. During the Vietnam War this reached a peak with much discussion about the ethics of this process. Proponents of the PIE and BICEPS principles argue that it leads to a reduction of long-term disability but opponents argue that combat stress reactions lead to long-term problems such as post-traumatic stress disorder.

The use of psychiatric drugs to treat victims of CSR has also attracted criticism, as some military psychiatrists have come to question the efficacy of such drugs on the long-term health of veterans. Concerns have been expressed as to the effect of pharmaceutical treatment on an already elevated substance abuse rate among former CSR sufferers.

Recent research has caused an increasing number of scientists to believe that there may be a physical (i.e. neurocerebral damage) rather than psychological basis for blast trauma. As traumatic brain injury and combat stress reaction have very different causes yet result in similar neurologic symptoms, researchers emphasize the need for greater diagnostic care.

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What is Acute Stress Disorder?

Introduction

Acute stress disorder (ASD, also known as acute stress reaction, psychological shock, mental shock, or simply shock) is a psychological response to a terrifying, traumatic or surprising experience.

It may bring about delayed stress reactions (better known as post-traumatic stress disorder, PTSD) if not correctly addressed.

Refer to Combat Stress Reaction.

Brief History

The term “acute stress disorder” was first used to describe the symptoms of soldiers during World War I and II, and it was therefore also termed “combat stress reaction” (CSR). Approximately 20% of US troops displayed symptoms of CSR during WWII. It was assumed to be a temporary response of healthy individuals to witnessing or experiencing traumatic events. Symptoms include depression, anxiety, withdrawal, confusion, paranoia, and sympathetic hyperactivity.

The American Psychological Association (APA) officially included the term ASD in the DSM-IV in 1994. Before that, symptomatic individuals within the first month of trauma were diagnosed with adjustment disorder. According to the DSM-IV, acute stress reaction refers to the symptoms experienced immediately to 48 hours after exposure to a traumatic event. In contrast, acute stress disorder is defined by symptoms experienced 48 hours to one month following the event. Symptoms experienced for longer than one month are consistent with a diagnosis of PTSD.

Initially, being able to describe different ASRs was one of the goals of introducing ASD. Some criticisms surrounding ASD’s focal point include issues with ASD recognising other distressing emotional reactions, like depression and shame. Emotional reactions similar to these may then be diagnosed as adjustment disorder under the current system of trying to diagnose ASD.

Since its addition to the DSM-IV, questions about the efficacy and purpose of the ASD diagnosis have been raised. The diagnosis of ASD was criticised as an unnecessary addition to the progress of diagnosing PTSD, as some considered it more akin to a sign of PTSD than an independent issue requiring diagnosis. Also, the terms ASD and ASR have been criticised for not fully covering the range of stress reactions.

Types of ASD

Sympathetic (also known as “Fight or Flight” Response)

Sympathetic acute stress disorder is caused by the release of excessive adrenaline and norepinephrine into the nervous system. These hormones may speed up a person’s pulse and respiratory rate, dilate pupils, or temporarily mask pain. This type of ASD developed as an evolutionary advantage to help humans survive dangerous situations. The “fight or flight” response may allow for temporarily-enhanced physical output, even in the face of severe injury. However, other physical illnesses become more difficult to diagnose, as ASD masks the pain and other vital signs that would otherwise be symptomatic.

Parasympathetic

Parasympathetic acute stress disorder is characterised by feeling faint and nauseous. This response is fairly often triggered by the sight of blood. In this stress response, the body releases acetylcholine. In many ways, this reaction is the opposite of the sympathetic response, in that it slows the heart rate and can cause the patient to either regurgitate or temporarily lose consciousness. The evolutionary value of this is unclear, although it may have allowed for prey to appear dead to avoid being eaten.

Signs and Symptoms

The DSM-IV specifies that acute stress disorder must be accompanied by the presence of dissociative symptoms, which largely differentiates it from PTSD.

Dissociative symptoms include a sense of numbing or detachment from emotional reactions, a sense of physical detachment – such as seeing oneself from another perspective – decreased awareness of one’s surroundings, the perception that one’s environment is unreal or dreamlike, and the inability to recall critical aspects of the traumatic event (dissociative amnesia).

In addition to these characteristics, ASD can be present in the following four distinct symptom clusters;

  • Intrusion symptom cluster:
    • Recurring and distressing dreams, flashbacks, and/or memories related to the traumatic event.
    • Intense/prolonged psychological distress or somatic reactions to internal or external traumatic cues.
  • Negative mood cluster:
    • A persistent inability to experience positive emotions such as happiness, loving feelings, or satisfaction.
  • Avoidance symptom cluster:
    • The avoidance of distressing memories, thoughts, feelings (or external reminders of them) that are closely associated with the traumatic event.
  • Arousal symptom cluster:
    • Sleep disturbances, hyper-vigilance, difficulties with concentration, easily startled, and irritability/anger/aggression.

Potential Developments

There are a number of issues that can arise from acute stress. Depression, anxiety, mood disorders, and substance abuse problems can develop from acute stress. Untreated ASD can also lead to the development of PTSD.

Causes

There are several theoretical perspectives on trauma response, including cognitive, biological, and psycho-biological. While PTSD-specific, these theories are still useful in understanding acute stress disorder, as the two disorders share many symptoms. A recent study found that even a single stressful event may have long-term consequences on cognitive function. This result calls the traditional distinction between the effects of acute and chronic stress into question.

Pathophysiology

Stress is characterised by specific physiological responses to adverse or noxious stimuli.

Hans Selye was the first to coin the term “general adaptation syndrome” to suggest that stress-induced physiological responses proceed through the stages of alarm, resistance, and exhaustion.

The sympathetic branch of the autonomic nervous system gives rise to a specific set of physiological responses to physical or psychological stress. The body’s response to stress is also termed a “fight or flight” response, and it is characterised by an increase in blood flow to the skeletal muscles, heart, and brain, a rise in heart rate and blood pressure, dilation of pupils, and an increase in the amount of glucose released by the liver.

The onset of an acute stress response is associated with specific physiological actions in the sympathetic nervous system, both directly and indirectly through the release of adrenaline and, to a lesser extent, noradrenaline from the medulla of the adrenal glands. These catecholamine hormones facilitate immediate physical reactions by triggering increases in heart rate and breathing, constricting blood vessels. An abundance of catecholamines at neuroreceptor sites facilitates reliance on spontaneous or intuitive behaviours often related to combat or escape.

Normally, when a person is in a serene, non-stimulated state, the firing of neurons in the locus ceruleus is minimal. A novel stimulus, once perceived, is relayed from the sensory cortex of the brain through the thalamus to the brain stem. That route of signalling increases the rate of noradrenergic activity in the locus ceruleus, and the person becomes more alert and attentive to their environment.

If a stimulus is perceived as a threat, a more intense and prolonged discharge of the locus ceruleus activates the sympathetic division of the autonomic nervous system. The activation of the sympathetic nervous system leads to the release of norepinephrine from nerve endings acting on the heart, blood vessels, respiratory centres, and other sites. The ensuing physiological changes constitute a major part of the acute stress response. The other major player in the acute stress response is the hypothalamic-pituitary-adrenal axis. Stress activates this axis and produces neuro-biological changes. These chemical changes increase the chances of survival by bringing the physiological system back to homeostasis.

The autonomic nervous system controls all automatic functions in the body and contains two subsections within it that aid the response to an acute stress reaction. These two subunits are the sympathetic nervous system and the parasympathetic nervous system. The sympathetic response is colloquially known as the “fight or flight” response, indicated by accelerated pulse and respiration rates, pupil dilation, and a general feeling of anxiety and hyper-awareness. This is caused by the release of epinephrine and norepinephrine from the adrenal glands. The epinephrine and norepinephrine strike the beta receptors of the heart, which feeds the heart’s sympathetic nerve fibres to increase the strength of heart muscle contraction; as a result, more blood gets circulated, increasing the heart rate and respiratory rate. The sympathetic nervous system also stimulates the skeletal system and muscular system to pump more blood to those areas to handle the acute stress. Simultaneously, the sympathetic nervous system inhibits the digestive system and the urinary system to optimise blood flow to the heart, lungs, and skeletal muscles. This plays a role in the alarm reaction stage. The parasympathetic response is colloquially known as the “rest and digest” response, indicated by reduced heart and respiration rates, and, more obviously, by a temporary loss of consciousness if the system is fired at a rapid rate. The parasympathetic nervous system stimulates the digestive system and urinary system to send more blood to those systems to increase the process of digestion. To do this, it must inhibit the cardiovascular system and respiratory system to optimise blood flow to the digestive tract, causing low heart and respiratory rates. The parasympathetic nervous system plays no role in acute stress response.

Studies have shown that patients with acute stress disorder have overactive right amygdalae and prefrontal cortices; both structures are involved in the fear-processing pathway.

Diagnosis

According to the DSM-V, symptom presentation must last for three consecutive days to be classified as acute stress disorder. If symptoms persist past one month, the diagnosis of PTSD is explored. There must be a clear temporal connection between the impact of an exceptional stressor and the onset of symptoms; onset is usually within a few minutes or days but may occur up to one month after the stressor. Also, the symptoms show a mixed and rapidly changing picture; although “daze” depression, anxiety, anger, despair, hyper-activity, and withdrawal may all be seen, no one symptom dominates for long. The symptoms usually resolve rapidly where removal from the stressful environment is possible. In cases where the stress continues, the symptoms usually begin to diminish after 24-48 hours and are usually minimal after about three days.

Evaluation of patients is done through close examination of emotional response. Using self-report from patients is a large part of diagnosing ASD, as acute stress is the result of reactions to stressful situations.

The DSM-V specifies that there is a higher prevalence rate of ASD among females compared to males due to higher risk of experiencing traumatic events and neurobiological gender differences in stress response.

Treatment

This disorder may resolve itself with time or may develop into a more severe disorder, such as PTSD. However, results of Creamer, O’Donnell, and Pattison’s (2004) study of 363 patients suggests that a diagnosis of acute stress disorder had only limited predictive validity for PTSD. Creamer et al. found that re-experiences of the traumatic event and arousal were better predictors of PTSD. Early pharmacotherapy may prevent the development of post-traumatic symptoms. Additionally, early trauma-focused cognitive behavioural therapy (TF-CBT) for those with a diagnosis of ASD can protect an individual from developing chronic PTSD.

Studies have been conducted to assess the efficacy of counselling and psychotherapy for people with acute stress disorder. Cognitive behavioural therapy, which includes exposure and cognitive restructuring, was found to be effective in preventing PTSD in patients diagnosed with acute stress disorder with clinically significant results at six-month follow-up appointments. A combination of relaxation, cognitive restructuring, imaginal exposure, and in-vivo exposure was superior to supportive counselling. Mindfulness-based stress reduction programmes also appear to be effective for stress management.

The pharmacological approach has made some progress in lessening the effects of ASD. To relax patients and allow for better sleep, Prazosin can be given to patients, which regulates their sympathetic response. Hydrocortisone has shown some success as an early preventative measure following a traumatic event, typically in the treatment of PTSD.

In a wilderness context where counselling, psychotherapy, and cognitive behavioural therapy is unlikely to be available, the treatment for acute stress reaction is very similar to the treatment of cardiogenic shock, vascular shock, and hypovolemic shock; that is, allowing the patient to lie down, providing reassurance, and removing the stimulus that prompted the reaction. In traditional shock cases, this generally means relieving injury pain or stopping blood loss. In an acute stress reaction, this may mean pulling a rescuer away from the emergency to calm down or blocking the sight of an injured friend from a patient.

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What is Anosognosia?

Introduction

Anosognosia is a condition in which a person with a disability is cognitively unaware of having it due to an underlying physical or psychological (e.g. PTSD, Stockholm syndrome, schizophrenia, bipolar disorder, dementia) condition.

Anosognosia can result from physiological damage to brain structures, typically to the parietal lobe or a diffuse lesion on the fronto-temporal-parietal area in the right hemisphere, and is thus a neuropsychiatric disorder. A deficit of self-awareness, it was first named by the neurologist Joseph Babinski in 1914. Phenomenologically, anosognosia has similarities to denial, which is a psychological defence mechanism; attempts have been made at a unified explanation. Anosognosia is sometimes accompanied by asomatognosia, a form of neglect in which patients deny ownership of body parts such as their limbs. The term is from Ancient Greek ἀ- a-, ‘without’, νόσος nosos, ‘disease’ and γνῶσις gnōsis, ‘knowledge’. It is also considered a disorder that makes the treatment of the patient more difficult, since it may affect negatively the therapeutic relationship.

Causes

Relatively little has been discovered about the cause of the condition since its initial identification. Recent empirical studies tend to consider anosognosia a multi-componential syndrome or multi-faceted phenomenon. That is it can be manifested by failure to be aware of a number of specific deficits, including motor (hemiplegia), sensory (hemianaesthesia, hemianopia), spatial (unilateral neglect), memory (dementia), and language (receptive aphasia) due to impairment of anatomo-functionally discrete monitoring systems.

Anosognosia is relatively common following different causes of brain injury, such as stroke and traumatic brain injury; for example, anosognosia for hemiparesis (weakness of one side of the body) with onset of acute stroke is estimated at between 10% and 18%. However, it can appear to occur in conjunction with virtually any neurological impairment. It is more frequent in the acute than in the chronic phase and more prominent for assessment in the cases with right hemispheric lesions than with the left. Anosognosia is not related to global mental confusion, cognitive flexibility, other major intellectual disturbances, or mere sensory/perceptual deficits.

The condition does not seem to be directly related to sensory loss but is thought to be caused by damage to higher level neurocognitive processes that are involved in integrating sensory information with processes that support spatial or bodily representations (including the somatosensory system). Anosognosia is thought to be related to unilateral neglect, a condition often found after damage to the non-dominant (usually the right) hemisphere of the cerebral cortex in which people seem unable to attend to, or sometimes comprehend, anything on a certain side of their body (usually the left).

Anosognosia can be selective in that an affected person with multiple impairments may seem unaware of only one handicap, while appearing to be fully aware of any others. This is consistent with the idea that the source of the problem relates to spatial representation of the body. For example, anosognosia for hemiplegia may occur with or without intact awareness of visuo-spatial unilateral neglect. This phenomenon of double dissociation can be an indicator of domain-specific disorders of awareness modules, meaning that in anosognosia, brain damage can selectively impact the self-monitoring process of one specific physical or cognitive function rather than a spatial location of the body.

There are also studies showing that the manoeuvre of vestibular stimulation could temporarily improve both the syndrome of spatial unilateral neglect and of anosognosia for left hemiplegia. Combining the findings of hemispheric asymmetry to the right, association with spatial unilateral neglect, and the temporal improvement on both syndromes, it is suggested there can be a spatial component underlying the mechanism of anosognosia for motor weakness and that neural processes could be modulated similarly. There were some cases of anosognosia for right hemiplegia after left hemisphere damage, but the frequency of this type of anosognosia has not been estimated.

Anosognosia may occur as part of receptive aphasia, a language disorder that causes poor comprehension of speech and the production of fluent but incomprehensible sentences. A patient with receptive aphasia cannot correct his own phonetics errors and shows “anger and disappointment with the person with whom s/he is speaking because that person fails to understand her/him”. This may be a result of brain damage to the posterior portion of the superior temporal gyrus, believed to contain representations of word sounds. With those representations significantly distorted, patients with receptive aphasia are unable to monitor their mistakes. Other patients with receptive aphasia are fully aware of their condition and speech inhibitions, but cannot monitor their condition, which is not the same as anosognosia and therefore cannot explain the occurrence of neologistic jargon.

Psychiatry

Although largely used to describe unawareness of impairment after brain injury or stroke, the term “anosognosia” is occasionally used to describe the lack of insight shown by some people with anorexia nervosa. They do not seem to recognise that they have a mental illness. There is evidence that anosognosia related to schizophrenia may be the result of frontal lobe damage. E. Fuller Torrey, a psychiatrist and schizophrenia researcher, has stated that among those with schizophrenia and bipolar disorder, anosognosia is the most prevalent reason for not taking medications.

Diagnosis

Clinically, anosognosia is often assessed by giving patients an anosognosia questionnaire in order to assess their metacognitive knowledge of deficits. However, neither of the existing questionnaires applied in the clinics are designed thoroughly for evaluating the multidimensional nature of this clinical phenomenon; nor are the responses obtained via offline questionnaire capable of revealing the discrepancy of awareness observed from their online task performance. The discrepancy is noticed when patients showed no awareness of their deficits from the offline responses to the questionnaire but demonstrated reluctance or verbal circumlocution when asked to perform an online task. For example, patients with anosognosia for hemiplegia may find excuses not to perform a bimanual task even though they do not admit it is because of their paralysed arms.

A similar situation can happen to patients with anosognosia for cognitive deficits after traumatic brain injury when monitoring their errors during the tasks regarding their memory and attention (online emergent awareness) and when predicting their performance right before the same tasks (online anticipatory awareness). It can also occur among patients with dementia and anosognosia for memory deficit when prompted with dementia-related words, showing possible pre-attentive processing and implicit knowledge of their memory problems. Patients with anosognosia may also overestimate their performance when asked in first-person formed questions but not from a third-person perspective when the questions referring to others.

When assessing the causes of anosognosia within stroke patients, CT scans have been used to assess where the greatest amount of damage is found within the various areas of the brain. Stroke patients with mild and severe levels of anosognosia (determined by response to an anosognosia questionnaire) have been linked to lesions within the temporoparietal and thalamic regions, when compared to those who experience moderate anosognosia, or none at all. In contrast, after a stroke, people with moderate anosognosia have a higher frequency of lesions involving the basal ganglia, compared to those with mild or severe anosognosia.

Treatment

In regard to anosognosia for neurological patients, no long-term treatments exist. As with unilateral neglect, caloric reflex testing (squirting ice cold water into the left ear) is known to temporarily ameliorate unawareness of impairment. It is not entirely clear how this works, although it is thought that the unconscious shift of attention or focus caused by the intense stimulation of the vestibular system temporarily influences awareness. Most cases of anosognosia appear to simply disappear over time, while other cases can last indefinitely. Normally, long-term cases are treated with cognitive therapy to train patients to adjust for their inoperable limbs (though it is believed that these patients still are not “aware” of their disability). Another commonly used method is the use of feedback – comparing clients’ self-predicted performance with their actual performance on a task in an attempt to improve insight.

Neurorehabilitation is difficult because, as anosognosia impairs the patient’s desire to seek medical aid, it may also impair their ability to seek rehabilitation. A lack of awareness of the deficit makes cooperative, mindful work with a therapist difficult. In the acute phase, very little can be done to improve their awareness, but during this time, it is important for the therapist to build a therapeutic alliance with patients by entering their phenomenological field and reducing their frustration and confusion. Since severity changes over time, no single method of treatment or rehabilitation has emerged or will likely emerge.

In regard to psychiatric patients, empirical studies verify that, for individuals with severe mental illnesses, lack of awareness of illness is significantly associated with both medication non-compliance and re-hospitalisation. Fifteen percent of individuals with severe mental illnesses who refuse to take medication voluntarily under any circumstances may require some form of coercion to remain compliant because of anosognosia. Coercive psychiatric treatment is a delicate and complex legal and ethical issue.

One study of voluntary and involuntary inpatients confirmed that committed patients require coercive treatment because they fail to recognise their need for care. The patients committed to the hospital had significantly lower measures of insight than the voluntary patients.

Anosognosia is also closely related to other cognitive dysfunctions that may impair the capacity of an individual to continuously participate in treatment. Other research has suggested that attitudes toward treatment can improve after involuntary treatment and that previously committed patients tend later to seek voluntary treatment.

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What is Logorrhoea?

Introduction

In psychology, logorrhea or logorrhoea (from Ancient Greek λόγος logos “word” and ῥέω rheo “to flow”), is a communication disorder that causes excessive wordiness and repetitiveness, which can cause incoherency.

Logorrhoea is sometimes classified as a mental illness, though it is more commonly classified as a symptom of mental illness or brain injury. This ailment is often reported as a symptom of Wernicke’s aphasia, where damage to the language processing centre of the brain creates difficulty in self-centred speech.

Refer to Tangential Speech.

Characteristics

Logorrhoea is characterised by the constant need to talk. Occasionally, patients suffering from logorrhoea may produce speech with normal prosody and a slightly fast speech rate. Other related symptoms include the use of neologisms (new words without clear derivation, e.g. hipidomateous for hippopotamus), words that bear no apparent meaning, and, in some extreme cases, the creation of new words and morphosyntactic constructions. From the “stream of unchecked nonsense often under pressure and the lack of self-correction” that the patient may exhibit, and their circumlocution (the ability to talk around missing words) we may conclude that they are unaware of the grammatical errors they are making.

Examples of Logorrhoea

When a clinician said, “Tell me what you do with a comb”, to a patient suffering from mild Wernicke’s aphasia (which produces the symptom of logorrhoea), the patient responded:

“What do I do with a comb … what I do with a comb. Well a comb is a utensil or some such thing that can be used for arranging and rearranging the hair on the head both by men and by women. One could also make music with it by putting a piece of paper behind and blowing through it. Sometimes it could be used in art – in sculpture, for example, to make a series of lines in soft clay. It’s usually made of plastic and usually black, although it comes in other colors. It is carried in the pocket or until it’s needed, when it is taken out and used, then put back in the pocket. Is that what you had in mind?”

In this case, the patient maintained proper grammar and did not exhibit any signs of neologisms. However, the patient did use an overabundance of speech in responding to the clinician, as most people would simply respond, “I use a comb to comb my hair.”

In a more extreme version of logorrhoea aphasia, a clinician asked a male patient, also with Wernicke’s aphasia, what brought him to the hospital. The patient responded:

“Is this some of the work that we work as we did before? … All right … From when wine [why] I’m here. What’s wrong with me because I … was myself until the taenz took something about the time between me and my regular time in that time and they took the time in that time here and that’s when the time took around here and saw me around in it’s started with me no time and I bekan [began] work of nothing else that’s the way the doctor find me that way…”

In this example, the patient’s aphasia was much more severe. Not only was this a case of logorrhoea, but this included neologisms (such as “taenz” for “stroke” and “regular time” for “regular bath”) and a loss of proper sentence structure.

Causes

Logorrhoea has been shown to be associated with traumatic brain injuries in the frontal lobe[7] as well as with lesions in the thalamus] and the ascending reticular inhibitory system and has been associated with aphasia. Logorrhoea can also result from a variety of psychiatric and neurological disorders including tachypsychia, mania, hyperactivity, catatonia, ADHD and schizophrenia.

Aphasias

Wernicke’s Aphasia, amongst other aphasias, are often associated with logorrhoea. Aphasia refers to the neurological disruption of language that occurs as a consequence of brain dysfunction. For a patient to truly have an aphasia, they cannot have been diagnosed with any other medical condition that may affect their cognition. Logorrhoea is a common symptom of Wernicke’s Aphasia, along with circumlocution, paraphasias, and neologisms. Often a patient with aphasia may present all of these symptoms at one time.

Treatment

Excessive talking may be a symptom of an underlying illness and should be addressed by a medical provider if combined with hyperactivity or symptoms of mental illness, such as hallucinations. Treatment of logorrhoea depends on its underlying disorder, if any. Antipsychotics are often used, and lithium is a common supplement given to manic patients. For patients with lesions of the brain, attempting to correct their errors may upset and anger the patients, since the language centre of their brain may not be able to process that what they are saying is incorrect and wordy.

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What is Tangential Speech?

Introduction

Tangential speech or tangentiality is a communication disorder in which the train of thought of the speaker wanders and shows a lack of focus, never returning to the initial topic of the conversation.

It tends to occur in situations where a person is experiencing high anxiety, as a manifestation of the psychosis known as schizophrenia, in dementia or in states of delirium. It is less severe than logorrhoea and may be associated with the middle stage in dementia. It is, however, more severe than circumstantial speech in which the speaker wanders, but eventually returns to the topic.

Some adults with right hemisphere brain damage may exhibit behaviour that includes tangential speech. Those who exhibit these behaviours may also have related symptoms such as seemingly inappropriate or self-centred social responses, and a deterioration in pragmatic abilities (including appropriate eye contact as well as topic maintenance).

Brief History

The earlier phenomenological description allowed for further definition on the basis of formal characteristic rather than content, producing later practice relying upon clinical assessment. The term has undergone a re-definition to refer only to a persons speech in response to a question, and to provide the definition separation from the similar symptoms loosening of association and derailment.

Definition

The term refers simplistically to a thought disorder shown from speech with a lack of observance to the main subject of discourse, such that a person whilst speaking on a topic deviates from the topic. Further definition is of speech that deviates from an answer to a question that is relevant in the first instance but deviates from the relevancy to related subjects not involved in a direct answering of the question. In the context of a conversation or discussion the communication is a response that is ineffective in that the form is inappropriate for adequate understanding. The person’s speech seems to indicate that their attention to their own speech has perhaps in some way been overcome during the occurrence of cognition whilst speaking, causing the vocalised content to follow thought that is apparently without reference to the original idea or question; or the person’s speech is considered evasive in that the person has decided to provide an answer to a question that is an avoidance of a direct answer.

Other

According to the St. Louis system for the diagnosis of schizophrenia, tangentiality is significantly associated with a low IQ prior to diagnosis.

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What is Organic Personality Disorder?

Introduction

Organic personality disorder (OPD), irrespective of the apparent nomenclature, is not included in the group of personality disorders.

For this reason, the symptoms and diagnostic criteria of the organic personality disorder are different from those of the other mental health disorders included in this various group. According to the Tenth Revision of the International Classification of Diseases (ICD-10) organic personality disorder is associated with a “significant alteration of the habitual patterns of premorbid behaviour”. There are crucial influences on emotions, impulses and personal needs because of this disorder.

Thus, all these definitions about the organic personality disorder support that this type of disorder is associated with changes in personality and behaviour.

Causes

Organic personality disorder is associated with “personality change due to general medical condition”. The organic personality disorder is included in a wide group of personality and behavioural disorders. This mental health disorder can be caused by disease, brain damages or dysfunctions in specific brain areas in frontal lobe. The most common reason for this profound change in personality is the traumatic brain injury (TBI). Children, whose brain areas have been injured or damaged, may present attention deficit hyperactivity disorder (ADHD), oppositional defiant disorder (ODD) and organic personality disorder. Moreover, this disorder is characterised as “frontal lobe syndrome”. This characteristic name shows that the organic personality disorder can usually be caused by lesions in three brain areas of frontal lobe. Specifically, the symptoms of organic personality disorder can also be caused by traumatic brain injuries in orbitofrontal cortex, anterior cingulate cortex and dorsolateral prefrontal cortex. It is worth mention that organic personality disorder may also be caused by lesions in other circumscribed brain areas.

Diagnosis and Symptoms

The ICD-10 includes a diagnostic guideline for the wide group of personality and behavioural disorders. However, every disorder has its own diagnostic criteria. In case of the organic personality disorder, patient has to show at least three of the following diagnostic criteria over a six or more months period. Organic personality disorder is associated with a large variety of symptoms, such as deficits in cognitive function, dysfunctional behaviours, psychosis, neurosis, emotional changes, alterations in expression function and irritability. Patients with organic personality disorder can present emotional lability that means their emotional expressions are unstable and fluctuating. In addition, patients show reduction in ability of perseverance with their goals and they express disinhibited behaviours, which are characterised by inappropriate sexual and antisocial actions. For instance, patients can show dissocial behaviours, like stealing. Moreover, according to diagnostic guideline of ICD-10, patients can suffer from cognitive disturbances and they present signs of suspiciousness and paranoid ideas. Additionally, patients may present alteration in process of language production that means there are changes in language rate and flow. Furthermore, patients may show changes in their sexual preference and hyposexuality symptoms.

Another common feature of personality of patients with organic personality disorder is their dysfunctional and maladaptive behaviour that causes serious problems in these patients, because they face problems with pursuit and achievement of their goals. It is worth to be mentioned that patients with organic personality disorder express a feeling of unreasonable satisfaction and euphoria. Also, the patients show aggressive behaviours sometimes and these serious dysfunctions in their behaviour can have effects on their life and their relationships with other people. Specifically patients show intense signs of anger and aggression because of their inability to handle their impulses. The type of this aggression is called “impulsive aggression”. Furthermore, it is worth to be mentioned that the pattern of organic personality disorder presents some similarities with pattern of temporal lobe epilepsy (TLE). Specifically patients who suffer from this chronic disorder type of epilepsy, express aggressive behaviours, likewise it happens to patients with organic personality disorder. Another similar symptom between Temporal lobe epilepsy and organic personality disorder is the epileptic seizure. The symptom of epileptic seizure has influence on patients’ personality that means it causes behavioural alterations”. The Temporal lobe epilepsy (TLE) is associated with the hyperexcitability of the medial temporal lobe (MTL) of patients. Finally, patients with organic personality disorder may present similar symptoms with patients, who suffer from the Huntington’s disease as well. The symptoms of apathy and irritability are common between these two groups of patients.

Treatment

As it has already been mentioned, patients with organic personality disorder show a wide variety of sudden behavioural changes and dysfunctions. There are not a lot of information about the treatment of this mental health disorder. The pharmacological approach is the most common therapy among patients with organic personality disorder. However, the choice of drug therapy relies on the seriousness of patient’s situation and what symptoms are shown. The choice and administration of specific drugs contribute to the reduction of symptoms of organic personality disorder. For this reason, it is crucial for patients’ treatment to be assessed by clinical psychologists and psychiatrists before the administration of drugs.

Additionally, the dysfunctions in expression of behaviour of patients with organic personality disorder and the development of symptom of irritability, which are caused by aggressive and self-injurious behaviours, can be dealt with the administration of carbamazepine. Moreover, the symptoms of this disorder can be decreased by the administration of valproic acid. Also, emotional irritability and signs of depression can be dealt with the use of nortriptyline and low-dose thioridazine. Except from the symptom of irritability, patients express aggressive behaviours. At the onset of drug therapy for effective treatment of anger and aggression, the drug of carbamazepine, phenobarbital, benztropine (or benzatropine) and haloperidol can be administrated in order to reduce the symptoms of patients with organic personality disorder. In addition, the use of propranolol may decrease the frequent behaviours of rage attacks.

Finally, it is important for patients to take part in psychotherapy during drug therapy. In this way, many of the adverse effects of the medications, both physiological and behavioural, can be lessened or avoided entirely. Furthermore, the clinicians can provide useful and helpful support to patients during these psychotherapy sessions. Thus, the combination of drug therapy with psychotherapy can lead to the reduction of symptoms of this disorder and the improvement of patients’ situation.

What is Impulse-Control Disorder?

Introduction

Impulse-control disorder (ICD) is a class of psychiatric disorders characterised by impulsivity – failure to resist a temptation, an urge, or an impulse; or having the inability to not speak on a thought.

Many psychiatric disorders feature impulsivity, including substance-related disorders, behavioural addictions, attention deficit hyperactivity disorder, foetal alcohol spectrum disorders, antisocial personality disorder, borderline personality disorder, conduct disorder and some mood disorders.

The fifth edition of the American Psychiatric Association’s Diagnostic and statistical manual of mental disorders (DSM-5) that was published in 2013 includes a new chapter (not in DSM-IV-TR) on disruptive, impulse-control, and conduct disorders covering disorders “characterized by problems in emotional and behavioral self-control”. Five behavioural stages characterise impulsivity:

  • An impulse;
  • Growing tension;
  • Pleasure on acting;
  • Relief from the urge; and
  • Finally guilt (which may or may not arise).

Types

Disorders characterised by impulsivity that were not categorised elsewhere in the DSM-IV-TR were also included in the category “Impulse-control disorders not elsewhere classified”. Trichotillomania (hair-pulling) and skin-picking were moved in DSM-5 to the obsessive-compulsive chapter. Additionally, other disorders not specifically listed in this category are often classed as impulsivity disorders. Terminology was changed in the DSM-V from “Not Otherwise Classified” to “Not Elsewhere Classified”.

Sexual Compulsion

Sexual compulsion includes an increased urge in sexual behaviour and thoughts. This compulsion may also lead to several consequences in the individual’s life, including risky partner selection, increased chance for STIs and depression, as well as unwanted pregnancy. There has not yet been a determined estimate of its prevalence due to the secretiveness of the disorder. However, research conducted in the early 1990s in the United States gave prevalence estimates between 5-6% in the US population, with male cases being higher than female.

Internet Addiction

The disorder of Internet addiction has only recently been taken into consideration and has been added as a form of ICD. It is characterised by excessive and damaging usage of Internet with increased amount of time spent chatting, web surfing, gambling, shopping or consuming pornography. Excessive and problematic Internet use has been reported across all age, social, economic, and educational ranges. Although initially thought to occur mostly in males, increasing rates have been also observed in females. However, no epidemiological study has been conducted yet to understand its prevalence.

Compulsive Shopping

Compulsive shopping or buying is characterised by a frequent irresistible urge to shop even if the purchases are not needed or cannot be afforded. The prevalence of compulsive buying in the US has been estimated to be 2-8% of the general adult population, with 80-95% of these cases being females. The onset is believed to occur in late teens or early twenties and the disorder is considered to be generally chronic.

Pyromania

Pyromania is characterised by impulsive and repetitive urges to deliberately start fires. Because of its nature, the number of studies performed for fire-setting are understandably very few. However, studies done on children and adolescents suffering from pyromania have reported its prevalence to be between 2.4 and 3.5% in the United States. It has also been observed that the incidence of fire-setting is more common in juvenile and teenage boys than girls of the same age.

Intermittent Explosive Disorder

Intermittent explosive disorder or IED is a clinical condition of experiencing recurrent aggressive episodes that are out of proportion of any given stressor. Earlier studies reported a prevalence rate between 1-2% in a clinical setting, however a study done by Coccaro and colleagues in 2004 had reported about 11.1% lifetime prevalence and 3.2% one month prevalence in a sample of a moderate number of individuals (n=253). Based on the study, Coccaro and colleagues estimated the prevalence of IED in 1.4 million individuals in the US and 10 million with lifetime IED.

Kleptomania

Kleptomania is characterised by an impulsive urge to steal purely for the sake of gratification. In the US the presence of kleptomania is unknown but has been estimated at 6 per 1000 individuals. Kleptomania is also thought to be the cause of 5% of annual shoplifting in the US If true, 100,000 arrests are made in the US annually due to kleptomaniac behaviour.

Signs and Symptoms

The signs and symptoms of impulse-control disorders vary based on the age of the persons suffering from them, the actual type of impulse-control that they are struggling with, the environment in which they are living, and whether they are male or female.

Co-Morbidity

Complications of late Parkinson’s disease may include a range of impulse-control disorders, including eating, buying, compulsive gambling, sexual behaviour, and related behaviours (punding, hobbyism and walkabout). Prevalence studies suggest that ICDs occur in 13.6-36.0% of Parkinson’s patients exhibited at least one form of ICD. There is a significant co-occurrence of pathological gambling and personality disorder, and is suggested to be caused partly by their common “genetic vulnerability”. The degree of heritability to ICD is similar to other psychiatric disorders including substance use disorder. There has also been found a genetic factor to the development of ICD just as there is for substance use disorder. The risk for subclinical PG in a population is accounted for by the risk of alcohol dependence by about 12-20% genetic and 3-8% environmental factors. There is a high rate of co-morbidity between ADHD and other impulse-control disorders.

Mechanism

Dysfunction of the striatum may prove to be the link between OCD, ICD and SUD. According to research, the ‘impulsiveness’ that occurs in the later stages of OCD is caused by progressive dysfunction of the ventral striatal circuit. Whereas in case of ICD and SUD, the increased dysfunction of dorsal striatal circuit increases the “ICD and SUD behaviours that are driven by the compulsive processes”. OCD and ICD have traditionally been viewed as two very different disorders, the former one is generally driven by the desire to avoid harm whereas the latter one driven “by reward-seeking behaviour”. Still, there are certain behaviours similar in both, for example the compulsive actions of ICD patients and the behaviour of reward-seeking (for example hoarding) in OCD patients.

Treatment

Impulse-control disorders have two treatment options: psychosocial and pharmacological. Treatment methodology is informed by the presence of comorbid conditions.

Medication

In the case of pathological gambling, along with fluvoxamine, clomipramine has been shown effective in the treatment, with reducing the problems of pathological gambling in a subject by up to 90%. Whereas in trichotillomania, the use of clomipramine has again been found to be effective, fluoxetine has not produced consistent positive results. Fluoxetine, however, has produced positive results in the treatment of pathological skin picking disorder, although more research is needed to conclude this information. Fluoxetine has also been evaluated in treating IED and demonstrated significant improvement in reducing frequency and severity of impulsive aggression and irritability in a sample of 100 subjects who were randomised into a 14-week, double-blind study. Despite a large decrease in impulsive aggression behaviour from baseline, only 44% of fluoxetine responders and 29% of all fluoxetine subjects were considered to be in full remission at the end of the study. Paroxetine has shown to be somewhat effective although the results are inconsistent. Another medication, escitalopram, has shown to improve the condition of the subjects of pathological gambling with anxiety symptoms. The results suggest that although SSRIs have shown positive results in the treatment of pathological gambling, inconsistent results with the use of SSRIs have been obtained which might suggest a neurological heterogeneity in the ICD spectrum.

Psychosocial

The psychosocial approach to the treatment of ICDs includes cognitive behavioural therapy (CBT) which has been reported to have positive results in the case of treatment of pathological gambling and sexual addiction. There is general consensus that cognitive-behavioural therapies offer an effective intervention model.

TypeDescription
Pathological GamblingSystematic desensitisation, aversive therapy, covert sensitisation, imaginal desensitisation, and stimulus control have been proven to be successful in the treatments to the problems of pathological gambling. Also, “cognitive techniques such as psychoeducation, cognitive-restructuring, and relapse prevention” have proven to be effective in the treatments of such cases.
PyromaniaPyromania is harder to control in adults due to lack of co-operation; however, CBT is effective in treating child pyromaniacs.
Intermittent Explosive DisorderAlong with several other methods of treatments, cognitive behavioural therapy has also shown to be effective in the case of Intermittent explosive disorder as well. Cognitive Relaxation and Coping Skills Therapy (CRCST), which consists of 12 sessions starting first with the relaxation training followed by cognitive restructuring, then exposure therapy is taken. Later, the focus is on resisting aggressive impulses and taking other preventative measures.
KleptomaniaIn the case of kleptomania, the cognitive behaviour techniques used in these cases consists of covert sensitisation, imaginal desensitisation, systematic desensitisation, aversion therapy, relaxation training, and “alternative sources of satisfaction”.
Compulsive BuyingAlthough compulsive buying falls under the category of Impulse-control disorder – Not Otherwise Specified in the DSM-IV-TR, some researchers have suggested that it consists of core features that represent impulse-control disorders which includes preceding tension, difficult to resist urges and relief or pleasure after action. The efficiency of cognitive behaviour therapy for compulsive buying is not truly determined yet; however, common techniques for the treatment include exposure and response prevention, relapse prevention, cognitive restructuring, covert sensitization, and stimulus control.