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my wife is abnormal psychology and our child is mental health awareness

#hey sorry for not posting any chapters or audiofiles i have like #literally just been absorbed in school #i have chem AND bio this semester it's killing me #anyway #graypost #shitpost

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So... what exactly are executive functioning supports...?

Planners, checklists, and reminders are definitely executive function supports, but they aren't the only things that are available. ...so, I've made a list of some examples. A thread (🧵)

Executive functioning includes so much, so executive function supports can be SO MANY things. Executive functions include decision making, working memory, task initiation, planning, prioritizing, many forms of self-regulation, and more.

So let's talk in broad categories

Category 1: Decisionmaking

Avoiding a decision altogether,

Choosing randomly,

Reducing the number of options to decide between,

Always doing the same decision (such as having a uniform for yourself),

Outsourcing decisions,

Having outside structure/expectations

Category 2: Working memory

Keeping things visible,

Reminders,

Collaborators who gently remind you of things,

Writing it down (i.e., notebooks, post-its, to-do lists, etc.),

External structure such as lunch hours,

Understanding why and how working memory fails

Category 3: Information processing

Avoiding weak processing areas (eg. reading for dyslexics like me)

Have information in multiple forms,

Make information processing context relevant,

Reduce incoming information or competing demands

Category 4: Task Management

Body doubling,

Transition time,

To-do lists,

Breaking tasks down (including people to help with that),

External structure for identify the next step,

clear, explicit instructions,

Schedules, planners, itineraries.

Category 5: Organization

Mind maps,

Labels, 

Notetaking templates,

Physical organizers,

Organizing methods (Kondo, Only 4 Things, etc.),

House cleaners, professional organizer, etc.

Clear bins,

An ability to toggle visibility

Category 6: Cognitive Flexibility

Transition time,

Pre-change warnings,

External support for identifying and reminding the new direction,

Context-based exemplars of similar change,

Visual schedules,

Reminders of when structure will start again

I've listed a lot of things here, but there are just so, so, so many more options.

Executive function supports can be ways that we think or approach situations (internal) or structures imposed on us by others (external). They can be physical tools that we can touch and interact with (tangible) or completely abstract ideas or approaches (intangible)

The big takeaways are that executive function supports can be any tool, structure, or communication that supports any of our executive functions.

Executive functioning struggles are core to the ADHD and autistic experiences (and secondary to other ND conditions). This means executive functioning takes a lot of energy for ADHD and/or autistic people, and the more support we have the more energy we can use for other things

So, yeah, planners, checklists, and reminders are definitely executive function supports, but so is a highschool bell schedule, hobby-related groups, professional services, and colleagues (consensually) harassing you to remember to send that email.

There are a lot of options!

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Hey! I got The Body Keeps The Score and The Haunted Self for christmas, and since neither of those are psychosis books (they're about trauma) I won't be doing write-ups about them (unless something is REALLY interesting to me). I do one book at a time though so you've all got ~500 more pages of Schizophrenia, Third Edition before the posts slow down for a bit!

#graypost

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I've been thinking of changing the way I view personality disorders by separating it into a "core" (inner world experience) and "adaptations" (behaviors) view, because the current DSM-5 model just treats it as if the adaptations are signs of the core, and I don't think that's necessarily true

Lacking empathy could be a sign of many personality disorders, but if it's because of an inner sense of superiority compensating for a deeper sense of inferiority it would be a narcissistic core, regardless of how many "narcissistic adaptations" it would present with, for example

Like if a person shuts down when presented with others' issues and becomes detached and cold when responding to it, with the inner belief/thought process that "they're detracting from me being the center of attention and admiration" and just goes quiet, you might consider that a schizoid adaptation to a narcissistic core under this approach

Though I'm just a highschool student who reads a lot with no professional training or experience or any data to back up if this would be useful in any way. It's just an idea to throw out there

#graypost #grayrambles #personality disorder #narcissistic personality disorder #schizoid personality disorder #low empathy #no empathy #npd #szpd #psychology #abnormal psychology

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Audiofile of previously posted chapters progress post

About half of people responded that they'd use audio! So here's that progress tracking post to which posts have had audio added to them. X means I have to do it, 'Done' means it's done and uploaded onto the post.

Psychosis, Trauma, and Dissociation: 1-4: Done 8: X 9: X 10: X 11: X 13: X 16: X 18: X 19: X 20: X 22: X 24: X 25: X

Schizophrenia, Third Edition: 1: X 2: X 3: X 4: X 5: X 6: X 8: X 9: X 10: X 11: X

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Chapter 11 of Schizophrenia, Third Edition: Environmental risk factors for schizophrenia

Nature VS. Nurture and "genetic" VS. "environmental" has been a long standing division in biomedical science. However, as we learn more about how inheritance meshes with non-inheritance this division becomes more doubtful. Basically, the human mind is complex and trying to sort out genetics from environmental influences is a challenge. However, progress is being made.

A lot of the research into environmental risk factors of schizophrenia is inspired by the hypothesis that schizophrenia is neurodevelopmental. Originally the hypothesis stated that genetics and environments interacted to have an impact on adult mental health, remaining "silent" or clinically dormant until after puberty due to maturational events leading to the emergence of schizophrenia symptoms. This hypothesis has been updated in response to new data over the years.

Schizophrenia used to be viewed as having an "equal incidence", but new studies and systematic reviews of existing data show that its incidence varies across time, between sites, and between groups, showing up to a five-fold worldwide variance in incidence according to a study by McGrath et al.

It is important to understand the taxonomy of risk factors. Variables that correlate with an outcome but do not precede it are not risk factors; variables that precede an outcome but are not causally related to that outcome are risk indicators. "Risk modifying factors" as a term should be reserved for factors that appear to operate within the causal chain - or contribute to the outcome. Risk factors can be both direct and indirect; risk modifying factors can have a wide variety of attributes (fixed or variable, endogenous or exogenous, protective or adverse, etc.)

There is a lot of evidence for the fact that children who go on to develop schizophrenia are subtly different from their peers in terms of motor/cognitive/social functioning. The Dunedin Birth Cohort Study followed 1037 children at the ages of 3-15 and assessed them again at the ages of 18, 21, and 26. It has helped to identify neurocognitive impairments in children who subsequently develop schizophrenia-like illnesses. Poorer motor development, poorer receptive language, and a lower IQ all increased the risk of developing schizophreniform disorder. Other groups have identified attention deficits and deficits in executive function are more prevalent among children who develop schizophrenia later in life.

The Dunedin cohort also provided clear evidence that children who develop schizophrenia are already showing "quasi-psychotic" phenomena by the end of the first decade of their life, such as believing people can read their mind, are spying on them, or are hearing voices. But, there is no evidence these are risk factors, rather they are risk indicators.

Early biological hazards: Interestingly enough, season of birth seems to be one of the most consistently replicated epidemiological feature of schizophrenia. There is a slight excess of births in the late winter to the spring, at least in the northern hemisphere. Possible factors playing into this are perinatal viral exposures and vitamin deficiencies, which are more common during the winter months.

There is robust evidence that pregnancy and birth complications have a significant effect in increasing the risk of later schizophrenia. Cannon et al. reported the following exposures were associated with increased risk: antepartum hemorrhage, diabetes, Rhesus incompatibility, pre-eclampsie, low birthweight, congenital malformations, reduced head circumference, uterine atony, asphyxia, and emergency ceserean section. Decreased hippocampal volume has also been observed in people with schizophrenia.

A number of studies that have been replicated show that schizophrenia is more common in those born to older fathers, with the age of the mother having no significant changes.

Amphetamine and methamphetamine can both cause schizo-phrenia like psychosis. Methamphetamine induced psychosis in particular mimicks the positive symptoms of schizophrenia very well. Genetic factors appear to play a role: those with no family history of schizophrenia could abuse the drug without developing psychosis, with those with greter familial predisposition were more likely to experience psychotic symptoms; those who developed psychosis were more likely to recover if they had no family history.

It's been long accepted that cannabis can cause brief psychotic episodes. With those who had established psychosis, those who continued to abuse it had worse outcomes. But does cannabis actually cause psychosis? Andreasson et al. examined and followed up almost 50000 young Swedish male conscripts, and found that men who had smoked cannabis by the age of conscription had double the risk for schizophrenia in the following 15 years. Those who smoked cannabis at least 50 times were six times as likely to later be diagnosed with it. There have been various studies and the reviews are all consistent with the idea that the greature exposure to cannabis, the greater the risk.

When it comes to social biology, several risk factors associated with schizophrenia can be conceptualized. Place of birth and upbringing has an impact: those born and/or raised in urban regions have an increased risk. One of the more striking findings is that schizophrenia risk is markedly increased in migrant groups, where recent systematic reviews have shown a consistent pattern in spite of concerns about validity.

While some of the findings for candidates of environmental risk factors for schizophrenia may be false leads, we should prepare ourselves for the list of potential environmental risk factors to lengthen even more.

#nerdpost #graypost #psychology #psychosis #schizophrenia #long post #book: schizophrenia third edition #tw drugs #drugs tw

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Would you be interested in an audio version of the chapter information I post?

This will come in the format of an audio file attached to the top of the post. It would be me reading it out loud with my blue snowball microphone. This would delay chapter posts, but increase accessibility of my blog.

I am not sure how I would implement this onto the site as I am just Not That Great with HTML yet, but I would figure it out somehow. If enough people are interested in this poll, all future chapter posts will include audio, and old chapter posts will eventually have them added (and I will have a pinned post tracking my progress for that, which will be deleted once all chapters have an audio file attached.)

#polls

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Chapter 10 of Schizophrenia, Third Edition: Schizophrenia - the epidemiological horizon

Establishing the epidemiological 'signature' of a disease (frequency in specific populations, geographical spread/spacial distributions, temporal variation, assocations with comorbid conditions and risk factors) is an essential step for discovering its causes and is a prerequisite for prevention and control. Attempts to do this with schizophrenia have not met with comparable success despite epidemiological investigations into the schizophrenia spectrum having been conducted for over a century. One major source of difficulty is the disease concept of schizophrenia itself, depending critically on self-reported subjective experiences and having an insufficiently understood underlying structural/functional pathology without an objective diagnostic test or validated biological marker. Despite the broad issues there is a general acceptance that schizophrenia is genetically complex, involving variants and mutations in multiple genes/gene networks, marked heterogeneity, and a significant non-genetic contribution to its phenotypic expression. Due to this, an epidemiological horizon would greatly help clinicians in making evidence-based diagnostic and treatment decisions.

Substantial percentages of people with the diagnosis of schizophrenia are in psychiatric hospital or outpatient populations, providing relatively easy access to cases for epidemiological investigation. However there are flaws to this, the probability of being in treatment varies place to place and clinical populations/hospital samples are rarely representative of all the people with a disorder. Because of the moving towards outpatient care, any case finding for schizophrenia that relies solely on hospital admissions is likely methodologically flawed. It's also estimated that about 17% of people with schizophrenia in the US never consult mental health services.

The descriptive epidemiology of schizophrenia still has gaps, but the overall picture has been laid down. The incidence rate of schizophrenia - the annual number of emerging new cases in a defined population per 1000 individuals at risk - is particularly interesting since it varies between causal and risk factors. Since there's no agreed upon 'inception' of schizophrenia, estimating the incidence is hard. The 'social' onset where behavioral abnormalities occur and a mental health consultation is made rarely coincides with the onset of the earliest symptoms enabling a diagnosis of the disorder, and the diagnostic symptoms are majority wise preceded by a prodromal phase that can be as long as 2-6 years. This problem is relatively unaddressed - many studies use the first hospital admission as an index of onset.

The prevalence of a disorder is the total number of cases per 1000 persons at risk present in a population at any given time or over a defined period - prevalence is a proportion, incidence is a rate. Most studies produce estimates that the range is about 0.50-1.60%, so the rule of thumb that schizophrenia occurs in about 1% of the population is not very far off.

Now to look at populations, very high rates of schizophrenia (two or three times the national or regional rate) have been reported for population isolates, such as an area in northern Sweden and several areas in Finland. Ever higher rates have been found on the Palau islands in the Pacific and in Daghestan, Northern Caucasus. At the other extreme, a near absense of schizophrenia has been observed in the Hutterites in South Dakota. Most studies report significantly higher rates of schizophrenia in more urban areas. This may reflect social and geographical drift rather than etiologically relevent causal processes as people in the prodromal phase may struggle with employment and affordable housing and thus move to inner city areas, but this is hypothetical.

Studies for years have shown that schizophrenia is associated with a high mortality rate, and a greater than 20% reduction in life expectancy in comparison to the general population. Unnatural causes (suicide, accidents, homicide) accounted for 25% of all deaths of people with psychoses over a 20-year period according to a study based on the Danish Psychiatric Case Register. In recent years the suicide rate in schizophrenia has become equal to or possibly higher than in major depression.

There is abundant evidence that schizophrenia may have its onset at almost any age, in childhood as well as past middle age, although the majority of onsets fall within the interval of 15-54 years of age. There is also no clear evidence of major or consistent sex differences in the symptoms of schizophrenia, and other consistent findings (shorter hospital stays and earlier remitting illness in women, less disability and higher survival rates in the community in women, etc) are also consistent with normal sexual dimorphism in brain development (as well as the possible neuro-protective role of estrogen.)

After nearly a century of epidemiological research, essential questions about the nature of schizophrenia are still unanswered. Two major conclusions stand out: 1) schizophrenia is robust and can be identified reliably in diverse populations, and 2) there is no single environmental risk factor of major effect on the incidence of schizophrenia that has been discovered so far.

#nerdpost #graypost #psychology #psychosis #schizophrenia #long post #book: schizophrenia third edition

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Chapter 9 of Schizophrenia, Third Edition: The secondary schizophrenias

Schizophrenia is a diagnosis of exclusion. There are no established tests that can explicitly confirm this disorder, and this was recognized by Kraepelin, Bleuler, and Schneider. The amount of brain disorders that can (uncommonly) cause schizophrenia-like symptoms presents a problem and an opportunity. On one hand it's a dilemma about the limits of the definition of schizophrenia, but on the other it can provide insight into biological mechanisms underlying schizophrenia symptoms.

In the past mental disorders were divided into the categories "organic" and "functional." In this framework schizophrenia was assigned to a class of disorders known as "functional psychoses" and this was used in the ICD-9. In the DSM-III and DSM-IIIR the term "organic" was redefined in an important way, so as to imply a specific pathological etiology, rather than to describe particular symptoms of a mental state. This led to a problem where "organic" psychoses were acknowledged to be essentially identical with schizophrenia and left the diagnostician in a spot of having to rename a syndrome whenever an organic cause became apparent. The DSM-IV and DSM-IVR attempted to rectify the problem by eliminating the section of a seperate category for "organic" mental disorders, and this artificial dichotomization is disappearing.

Basically, since the term "organic" has plenty of problems to it it's being phased out in favour of "secondary." In the context of schizophrenia, that makes for "primary schizophrenia" and "secondary to a non-psychiatric medical disorder." Secondary schizophrenias can fall into two categories: 1. Psychotic symptoms come from the cerebral involvement of a systemic illness known to affect the brain, or 2. Schizophrenic symptoms come in the context of a demonstratable neuropathologically defined disorder that is not part of an ongoing systemic disease process.

With the disputes in definition and diagnosis it's not surprising that little is known about secondary schizophrenias. A problem in estimating prevalence is in the definition, how confident can we be that the well-defined brain disease is really responsible for the schizophrenic symptoms? A second difficulty is that the closer we look the more likely structural pathology will be revealed.

For schizophrenia-like symptoms co-occuring with organic brain diseases, there is a lot to go over. The estimates of the incidence of schizophrenia like symptoms in temporal lobe epilepsy vary widely, and more refined studies may be promising to explore anatomical and physiological links between schizophrenic symptoms and epilepsy.

A number of studies have found that schizophrenia is increased in frequency after traumatic brain injury. Temporal lobe injury was most frequently associated with psychosis, and delusional disorder was the most common presentation. In another study it was estimated that the risk of psychosis after TBI was two to five times greater than in uninjured controls. More recent studies show that the incidence of schizophrenia is only moderately raised after head injury, and that pre-existing psychosis just predisposes to head injury.

For space-occupying lesions: Behavioral and mood disturbances usually follow, but schizophrenia-like symptoms are rare for intracranial tumors. Some patients experient transient, poorly formed visual hallucinations which suggest temporal lobe involvement. Schizophrenia-like symptoms were more common in tumors involving the temporal lobe and cingulate gyrus. Overall misdiagnosis of schizophrenia in those that actually have brain tumors is extremely rare.

For cerebrovascular disease: Short-lived paranoid delusional states that are often accompanied by confusion, affective and behavioral disturbances can be encountered in acute stroke. Delusional misidentification (reduplicative paramnesia, Capgras and Fregoli syndromes) experienced by these patients may be caused by a disconnection between brain areas specialized in face and place recognition. Visual hallucinations may reflect abnormalities in occipital neural circuits.

For movement disorders, psychotic symptoms are common in patients with Parkinson's disease. Nearly half of patients expereince visual hallucinations and they are more likely to occur in the elderly and in those with cognitive impairment or depression. Hallucinations are usually non-threatening, transient, and stereotyped images of people or animals, and tend to occur at night. Delusions are less frequent (about 10% of patients) but are often distressing. Themes of persecution, theft, phantom boarders, and infidelity are common. Dementia with Lewy bodies is an increasingly recognized form of dementia, and psychotic symptoms are one of its core features, occuring in half of patients. Visual hallucinations, misidentification and reduplications, and delusions have all been reported. Another disease to mention is Huntington disease as it is associated with an increased risk of schizophrenia - 5-11% of patients reported schizophrenia like symptoms.

For demyelinating diseases: Anxiety and depression are very common in multiple sclerosis, but psychotic symptoms are much less common. While the prevalence is 2-3% in multiple sclerosis, that's double that in a normal population, so there is an association between the two. Studies suggest that onset of psychosis usually occurs when multiple sclerosis is well established and that paranoid delusions and lack of insight are common. Schizophrenic symptoms may also present in other conditions where myelin development is interrupted, such as metachromatic leukodystrophy, adrenoleukodystrophy, cerebrotendinous zanthomatosis, Schlider, Niemann-Pick and Pelizaeus-Merzbacher diseases, and phenylketonuria.

Metabolic disorders rarely induce psychotic symptoms, more commonly they are associated with depression or delirium. Thyroid-related psychoses are usually affectively based.

Infections of the central nervous system usually cause delirium but occasionally cause psychosis. Limbic encephalitis is most often associated with psychotic symptoms. A variety of viruses causing encephalitis lead to psychotic symptoms: Epstein-Barr, cytomegalovirus, rubella, herpex simplex, and measles. Psychotic symptoms can arise in the context of HIV infection and AIDS as well.

Drug-related psychosis is another issue. Psychotic symptoms can be induced by a variety of drugs, but the link between schizophrenia and drug use is more complex. Drug use in schizophrenia is associated with earlier age of onset, more severe symptoms, more frequent relapses, and less compliance with medication. A study reported 60% drug use in patients with schizophrenia, 37% of which had a concurrent diagnosis of substance use disorder. Another study has suggested that in schizophrenia, pathology in reward circuits may increase vulnerability to addictions. Cannabis, alcohol, and cocaine alone or in combination were the substances most common in drug-induced psychosis groups. A survey in UK prisons found a five-fold increase in psychosis for cocaine users, three-fold for amphetamine users and two-fold for cannabis users.

#nerdpost #graypost #psychology #psychosis #schizophrenia #long post #book: schizophrenia third edition

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i reblogged a bunch of shit on another sideblog to add to my neocities site as resources and misc stuff and legit just forgot about it. whoops, will probably get around to that today

I also can't decide if after every chapter of Schizophrenia, Third Edition I should format the chapter write-up in HTML for my site, or if I actually want to sit and format the entire thing in one go for two hours once I finish the book. IDK, I enjoy mindless busiwork like that, it's a good distraction

#graypost #grayrambles

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Chapter 8 of Schizophrenia, Third Edition: Neurocognitive impairments

The data on cognitive functioning in schizophrenia has been remarkably uniform over many years. Since the start of Kraepelin and Bleuler, abnormalities in attention, associative, and volitional processes have been considered center to the disorder. Later in "Diagnostic Psychological Testing" by Rappaport et al., the greatest impairments in schizophrenia were noted to be judgement, attention, concentration, planning ability and anticipation. While these findings have stayed the same, what has changed in modern day is the significance attributed to the results.

The original observations by Kraepelin and Bleuler that cognitive impairments are central to the disorder have been supported by rich empirical research, like the work by Goldstein and Shakow and many others. To further investigate the question of whether observed impairment in brain function could be directly related to structural brain abnormalities, clinical neuropsychological methods became commonplace in the late 70s and 80s.

In addition to clinical neuropsychological literature, there is also a rich history of experimental studies that focus on specific cognitive functions. Three in particular have attracted great interest: episodic memory, working memory and attention.

In terms of episodic memory, both meta-analytic and experimental studies provide important evidence about the nature of memory impairment. First off, the impairment isn't modality-specific, with reliable deficits in both verbal and visual material. Secondly impairment is maximally evident using free recall methods. Third, the extent of patient impairment does not appear to be reliably amplified by increasing the delay interval between initial learning and later test. So, the deficit is better described as a problem with learning and acquiring information, rather than a deficit in memory.

There is growing evidence that the problem is in the initial learning or encoding of memory. That is, patients fail to initially process the material that allows for later memory retrieval. Some failures in encoding may result from failures to use strategic organizational processes that are typically thought to be mediated by non-medial temporal lobe structures.

For working memory, since literature demonstrates that it is a critical resource required by many different cognitive operations (reasoning, language comprehension, mental arithmetic), impairment in working memory would be expected to cause widespread impairments. Two main issues emerge. First, working memory effect sizes are not among the largest in the overall cognitive literature. Even if working memory is a critical resource for multiple cognitive processes, in order for working memory deficits to explain other impairments one would have to posit that the working memory deficit is somehow substantially amplified when in the context of other processes. Secondly, it is thought that working memory is the basis for executive control. However critical this is to working memory, it is not clear that much of the experimental work on the precision and capacity of working memory offers important traction in understanding higher-order working memory processes in relation to executive control.

On attention, patients tend to appear preoccupied or distracted by their own thoughts and perceptions, and have difficulty sustaining expected engagement with the external environment. There is abundant evidence of failures in the control of attention. Patients can have difficulty resisting having their attention brought to highly salient stimuli despite it being maladaptive to do so.

#nerdpost #graypost #psychology #psychosis #schizophrenia #long post #book: schizophrenia third edition #cognitive symptoms #i skipped chapter 7 #didn't wanna read it #lol

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Chapter 6 of Schizophrenia, Third Edition: The prodrome of schizophrenia

Typically, early psychosis work targets people presenting with a first episode of psychosis. However, there are identifiable signs and symptoms before psychosis has onset and there has been a worldwide movement to develop comprehensive early intervention programs for schizophrenia. Is it possible to intervene before the onset of the full disorder? Studies that focus on pre-onset are controversial because the development of a disorder remains a possibility.

Many that seek help during the prodromal phase are already debilitated by their symptoms despite them being sub-threshold for psychosis. Reducing the duration of untreated psychosis in the first episode may prevent or limit the future severity of symptoms, chronicity of the disorder, or resultant collateral damage. Many people who receive treatment for their psychotic symptoms and go into remission still find themselves disabled. It's believed this disability formed during the prodromal period.

For those with a psychotic illness, the prodrome is the time period where there is a change from a person's premorbid functioning up until obvious psychotic symptoms occur. 80-90% of patients with schizophrenia report a variety of symptoms including changes in perception, beliefs, cognition, mood, affect, and behavior that preceded psychosis.

Ideally providing treatment during the prodrome would delay or even prevent the transition into psychosis. Even if it can only delay the development of a psychotic episode, early intervention may minimize the impact that the episode has on functioning. However, in the absense of infallible markers of vulnerability the ethics of early intervention research needs to be seriously considered.

#nerdpost #graypost #psychology #psychosis #schizophrenia #book: schizophrenia third edition #prodrome #prodromal phase

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Chapter 5 of Schizophrenia, Third Edition: The schizophrenia spectrum persononality disorders

Classic studies by Kraepelin and Bleuler reported that schizophrenia is present in a continuum. The assessment of this disorder thus has included populations other than those with the disorder itself like relatives of patients with schizophrenia, subjects in prodromal stages, and people with schizophrenia spectrum personality disorders.

Schizotypal personality disorder (StPD) is the primary example of a schizophrenia spectrum personality disorder. Patients with the disorder share common genetic, biological, phenomenological, prognosis, and treatment response characteristics with people with schizophrenia. StPD shares with schizophrenia symptom dimensions such as ideas of reference, magical thinking, and suspiciousness, and deficit-like symptoms. Pervasive asociality and cognitive impairments observed in patients with StPD are usually milder than those with schizophrenia. People with StPD also do not suffer from chronic psychosis like those with schizophrenia do.

Individuals with StPD suffer from attenuated psychotic-like symptoms such as ideas of reference and cognitive-perceptual distortions as well as deficit-like symptoms such as constricted affect, social isolation, and peculiar appearance and speech. Ideas of reference in StPD are not held with the same conviction as in schizophrenia, but are nevertheless pervasive and disturbing. People with StPD also contemplate idiosyncratic beliefs that are not part of the social norms of their culture. One example is magical thinking, that the mind is able to change the physical world. They also experience illusions.

Studying StPD alongsize schizophrenia and healthy patients can allow us a further look at genetics and pathophysiology. Genes possibly related to schizophrenia are starting to be identified, and with that we can identify those that are related to both schizotypal and schizophrenia or just schizophrenia and psychosis along.

Individuals with schizoid personality disorder (SzPD) share the lack of close friends with StPD. However individuals with SzPD may not experience the cognitive-perceptual distortions that are criteria for StPD. Asociality is a core trait of SzPD, but in contrast in StPD it is not secondary to distrust of others, but just a desire to be alone due to a lack of pleasure from casual relationships.

In paranoid personality disorder (PPD) the diagnostic criteria has emphasis on the individual's mistrust and suspiciousness. The expectation of malicious intent from others and volatile responses to perceived slights comes from the perceived hidden threatening meanings that justify their preconceptions. People with PPD are also reluctant to confide in others since they question the loyalty of others and are even fearful of the ill-will of close friends.

Individuals with avoidant personality disorder (AvPD) may seem socially distant and exhibiy similar cognitive impairments to those observed in schizophrenia spectrum disorders, however, the critera emphasizes that this results not from lack of desire for relationships but from substantial anxiety and need for reassurance.

In some contexts, schizophrenia spectrum disorders are conceptualized as continuous or dimensional in nature. By some authors the common underlying liability shared between schizophrenia spectrum disorders is identified as "schizotaxia," that describes a set of signs and symptoms present in individuals genetically predisposed to schizophrenia.

Genes play a big role in schizophrenia. This genetic liability is not specific to schizophrenia - PPD, SzPD, and StPD are all associated with the genetic risk for schizophrenia. The strongest familial relationship to schizophrenia is with StPD, with the genetic relation between the two being suggested by several family and adoption studies.

Differences between schizophrenia and StPD are being examined with genetic, neurochemical, imaging, and pharmacological intruments.

#nerdpost #graypost #psychology #psychosis #schizophrenia #book: schizophrenia third edition #stpd #ppd #szpd #avpd #schizophrenia spectrum

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Chapter 4 of Schizophrenia, Third Edition: Late-onset schizophrenia

Schizophrenia has usually been thought of as having an onset in adolescence or early adulthood. However, there exists a distinct minority who have their onset in middle age and later. Some hesitate to call this schizophrenia and some accept the notion that a fixed age for developing schizophrenia may be arbitrary. Controversy about terminology continues. Both Kraepelin and Bleuler observed that there were patients who onset later in life and whose cases resembled those that onset in early adult life. Kraepelin reported that 5.6% of patients had onset after age 40, and Bleuler recorded between 15% and 17% for the same age.

Persecutory delusions usually dominate the picture. Delusions of reference (76%), control (25%), grandiose ability (12%), and hypochondrial nature (11%) were present as well. Usually, late onset cases represent the paranoid subtype, with disorganized and catatonic subtypes being very rare. While psychotic symptom presentation didn't differ that much from earlier onset cases, it was found that late onset cases had less severe negative symptoms.

There is a consistent finding that late-onset schizophrenia happens in women more often. There are several theories and propositions to why this happens but none of them have much proof behind them yet.

Even though patients with late-onset schizophrenia are often described as hostile and their relationships with neighbors/primary care physicians/police may be affected by their psychotic symptoms, the author's experience is that they are often very lonely. It's always possible to take the time to listen and offer sympathy to the patient's account of their persecution. Once a trusting relationship has been established patients will often accept medication and care.

Responses to typical antipsychotics were described as not effective as they could have been and 'modest.' There is a lack of research in the area of the effects of atypical antipsychotics. Since there is no evidence for any particular antipsychotic being better for this group of patients, medication should be chosen based on concomitant physical illness and other treatments received together with the specific side effects of the drug.

#nerdpost #graypost #psychology #psychosis #schizophrenia #book: schizophrenia third edition #late onset schizophrenia

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Chapter 3 of Schizophrenia, Third Edition: Child and adolescent schizophrenia

Although it's rare before the age of 10, childhood and adolescent schizophrenia does happen. Things like clinical severity, impact on development, and poor prognosis calls for a need of early detection, prompt diagnosis, and effective treatment. Childhood/adolescent onset schizophrenia is associated with poor premorbid functioning and early developmental delays, which is particularly striking for people with onset before adolescence. Similar impairments have been reported in adult-onset cases but are more common in child/adolescent-onset cases. These premorbid impairments may be a risk, or a precursor to psychosis. Diagnoses like anxiety, depression, ADHD, and autism may precede the diagnosis of schizophrenia in children and adolescents.

People who develop schizophrenia typically go through a prodromal phase characterized by a marked decline in functioning. Things like social withdrawal, decline in school performance, and uncharacteristic and odd behavior begin on average a year before the onset of psychotic symptoms. In retrospect things like non-specific behavioral changes were frequently early negative symptoms well before positive symptoms showed. Prodromal symptoms may also include odd ideas, eccentric interests, changes in affect, unusual experiences, and bizarre perceptual experiences. While these are characteristic of schizotypal personality disorder, in a schizophrenic prodrome there is usually a progression to a more severe dysfunction.

Child and adolescent-onset schizophrenia is characteristically chronic, with only a minority of cases making a full recovery. If full recovery does occur it is most likely in the first three months, and Hollis (1999) found that 12% of cases of schizophrenia only reached full remission. A Maudsley study found that those who were psychotic after 6 months have a 15% chance of full remission, while over half of cases who made a full recovery had active psychotic symptoms for less than 3 months. This indicates that observation past 6 months adds little new information, and the course over the first 6 months is the best predictor of remission.

A number of long-term follow-up studies of child and adolescent-onset schizophrenia all describe a chronic, unremitting long-term course with severely impaired functioning in adult life. Roughly one-fifth of cases in most studies have a good outcome while at the other extreme one-third are severely impaired. After the first few years of the illness there is little evidence of further progressive decline. Third, child and adolescent-onset schizophrenia has a worse outcome than adult-onset schizophrenia and affective psychoses. Social functioning is also very impaired in early onset schizophrenia. These findings confirm childhood schizophrenia is at an extreme end of a continuum of severity.

Cognitive symptoms of schizophrenia are increasingly being acknowledged as core features of the disorder. The degree of cognitive impairment is greater in child and adolescent-onset than adult-onset cases, which raises several questions. Are cognitive deficits specific or general - are some areas more affected? Which deficits precede psychosis and could be causal, and which are consequences of psychosis? Is it specific to schizophrenia or is it common between other developmental and psychotic disorders? Are cognitive impairments progressive or static after the onset of psychosis?

In summary of the findings: sensorimoter skills, associative memory, and simple language abilities are preserved in children with schizophrenia. Bigger decifits include tasks that require sustained and focused attention, flexible switching of cognitive set, high-information processing speed, and suppression of prepotent responses. These cognitive processes are executive functions, necessary for organizing goal-directed behavior.

Assessing a child or adolescent with schizophrenia should include detailed history, mental state and physical examination, and laboratory tests. Usually physical exams include a full blood count and biochemistry, including liver and thyroid function and a drug screen. Progressive structural brain changes indicate value in getting an MRI. Antipsychotics stay a cornerstone of treatment of schizophrenia but treatment should take a multimodal approach including pharmacotherapy, family and individual counselling, education about the illness, and provision to meet social/educational needs.

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Chapter 2 of Schizophrenia, Third Edition: The schizophrenia construct - symptomatic presentation

Most people with schizophrenia experience delusions and hallucinations, and many (but not all) experience disorganized thinking. There are also negative and cognitive symptoms.

For reality distortion, the delusions and hallucinations: A delusion is an unshakable, false idea or belief that cannot be attributed to the patient's educational, social, or cultural background, which is held with extraordinary conviction and subjective certainty, and is not amenable to logic. Delusions are divided into primary and secondary delusions: Primary delusions (more characteristic of schizophrenia) do not occur in response to something else such as a mood disorder or hallucination. Secondary delusions can be understood in relation to a person's background culture or emotional state.

Primary delusions include delusional perceptions and delusional intuitions. Delusional pereptions are normal perceptions that are interpreted with a delusonal meaning. Delusions are extremely variable in content. The most common delusions may be delusions of persecution, delusions of influence or control, thought withdrawal, thought insertion, thought broadcasting, morbid jealousy, erotomania, delusional misidentification, grandiose delusions, and religious delusions. In schizophrenia, the most common is delusions of persecution. The content of the delusion is often determined by the maturational, social, educational, and cultural background of the patient.

People with schizophrenia experience abnormal perceptions mainly in the form of sensory distortions - real objects are distorted - and false perceptions - where a new perception occurs. In false perceptions, there are illusions and hallucinations. Illusions are transformations of perceptions. Hallucinations are perceptions without object. Hallucinations can occur in any sense (auditory, visual, olfactory, gustatory and tactile, somatic or kinesthetic.) Around 50% of people with schizophrenia experience auditory hallucinations, 15% visual, and 5% tactile. The most common hallucinatory experience are hearing voices (also known as auditory verbal hallucinations.)

Now for disorganization: most people with schizophrenia have different degrees of impairment in their thought processes. These are called formal thought disorders. The ones most prominent in schizophrenia are called retardation (taking a long time to answer questions, in its extreme form, mutism occurs), circumstantiality (giving unnecesary details but eventually getting to the point), tangentiality (never getting to the point in the first place), derailment (breakdown in association with no logical connection between thoughts), thought blocking (sudden break in train of thought), and perseveration (repeating of an idea until it is inappropriate). There is also illogicality, offering bizarre explanations for things, neologisms, the creation of new words, and paraphasia, using a word with a new meaning.

In general negative symptoms are conceptualized as things that people do not do. The distinction between positive and negative symptoms was first introduced by Reynolds (1828-1896) and Jackson (1834-1911). Kraepelin (1919) also described a framework for distinguishing between positive and negative symptoms. In many cases negative symptoms are present before the onset of psychotic symptoms, present through the psychotic phase, and persist to varying degrees once the positive symptoms remit. Negative symptoms most often include alogia (poverty of speech), blunted affect (reduction in emotional expressiveness), anhedonia (inability to experience pleasure), asociality, avolition (lack of motivation), and apathy. Negative symptoms are more important for prognosis than positive symptoms.

Deficits in cognition have been considered core features of schizophrenia all the way back to Kraepelin and Bleuler. It's been consistently shown that people with schizophrenia have cognitive deficits right at the onset of psychotic symptoms, and even in the prodromal period or well before showing any kind of symptoms. There has been a lack of standard assessment scales for cognitive symptoms. Cognitive impairment is associated with poorer prognosis and functional outcome, negative symptoms, and disorganized symptoms, but not with positive symptoms.

Now on movement disorders: the two most common abnormal movements in schizophrenia are mannerisms (odd and stilted movements that seem to have a purpose) and stereotypy (constant repitition of meaningless movements.) People with schizophrenia may be stuporous, with an absence of movements and speech while being fully conscious. On the contrary, one might become hyperactive in an excited variety of catatonia. Sometimes there is abnormality in the execution of movements like in the form of negativism, automatic obedience, or ambitendency.

While those are the symptoms of schizophrenia, there are other aspects that are critical to evaluation and treatment. First of is the developmental history and prognostic indicators. Accurately diagnosing psychotic disorders is incredibly important at early stages of the disease because the importance of early treatment has been shown in different meaures. This variable is usually the level of social functioning prior to the onset of the illness, and it's been shown that it could be an important factor in diagnosis, diseae progression, and outcome.

All of feeling, mood, affect, and motivation can be abnormal in schizophrenia. The rate of depression in schizophrenia varies in studies, found more prevalent in women and patients with first-episode schizophrenia. People with comorbid schizophrenia and depression have poorer long term functional outcomes in terms of poorer quality of life. There is also "post schizophrenic depresson", which is depression following or in conjunction with psychotic symptoms (it's also a subtype in the ICD 10.) Depressive symptoms could also be confounded with antipsychotic side effects and negative symptoms. Suicide is unfortunately a leading cause of death in people with schizophrenia, with up to 40% of people with schizophrenia attempting suicide at least once. Between 5% and 13% die from their attempts. Risk factors for suicide in schizophrenia are comorbid depression and substance abuse, feelings of hopelessness and loss, fear of mental disintegration, a first episode (especially in previously high functioning patients), and periods of exacerbation of psychotic symptoms.

Substance abuse is common in schizophrenia. Half of patients are also substance abusers at some time during their illness. Substance use has been associated with poor social adjustment, more hospitalizations and relapses, medication and non-compliance, and poor treatment responses. Since acute intoxication and withdrawal of substances can mimick schizophrenic disorders, the overlap in symptoms can make diagnosis hard.

Now for physical health; the heightened health risks in schizophrenia (cardiovascular disease, metabolic syndrome, carbohydrate and lipid metabolid disorders, etc) are associated with the medications used in its treatment. Since people with schizophrenia show a higher rate of tobacco smoking than the general population, people with schizophrenia have more respiratory symptoms and poorer lung function compared to the general population. The presence of diabetes is between 9% and 14%, dyslipidemia 43%, and hypertension 30%. People with schizophrenia on antipsychotics are more prone to obesity, which has a big impact on both physical health and self-image and adherence to prescribed medication. Despite this vulnerability to different physical illnesses people with schizophrenia are at risk for failing to receive medical services. They should have routine physical examinations, and their physical symptoms should be explored no differently.

Extra tidbits: Sexual dysfunction, sleep problems, and eating disorders are also not uncommon in people with schizophrenia. Social functioning deficits are a hallmark of schizophrenia, and impairments in adaptive life skills are a major source of disability in people with schizophrenia. Quality of life is usually lower.

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Chapter 1 of Schizophrenia, Third Edition: Concept of schizophrenia - past, present, and future

Basically, try as psychologists might to define schizophrenia, even in the present its defintion stays ever-changing. Still, we need a working definition to provide a foundation for the study of the disease, so this will overview the history of concepts of psychosis and schizophrenia.

Although the name "schizophrenia" is relatively new, only being coined in the last century, the concept of psychosis is very old. Based on portrayals in early history and literature, we know that schizophrenia-like psychoses have been recognized since at least the first millenium BC. One of the earliest descriptions of a psychotic condition is in the book of Samuel in the Old Testament. After David successfully defends the Israelites against the Philistines by killing Goliath and then wins several subsequent battles, King Saul becomes increasingly paranoid about David's military prowess, planning and attempting to murder David. Saul even begins to have hallucinatory-like experiences.

Moving on to the classical era in Greece and Rome, there are plenty of descriptions regarding paranoid schizophrenia-like psychotic states. Greek tragedy has an abundance of portrayals of individuals tormented by psychosis, driven to committing horrendous acts. In "The Bacchae", Agave murders her son Pentheus, driven by the delusional belief that he is a lion. In "Medea", after Jason abandons his wife Medea, she falls into a psychotic rage that drives her to murder their two children. In "The Oresteia", Orestes is pursued by Furies until he finally loses reason and lapses into madness. And there are many more examples!

In the 16th and 17th centuries, Elizabethan and Jacobean drama are also filled with portrayals of individuals who experience schizophrenia-like psychotic states. Some of the best known are in the plays of Shakespeare - Hamlet, Lear, Othello, and Lady Macbeth all experience psychosis.

Not only were there literary portrayals documenting that schizophrenia-like illnesses have been present for at least three millennia, but the "medical" literature of these early times shows evidence that psychotic disorders similar to schizophrenia were recognized as important medical illnesses. They are described in the writings of Hippocrates, Galen, or Soranus or Ephesus. While the disorders described by these forefathers don't perfectly map onto modern classification systems, there are striking similarities. Mental illnesses were clearly seen as physical in origin. There were five groups of illness: melancholia, phrenitis, mania, hysteria, and epilepsy. Mania was essentially equivalent to our concept of psychosis. However, psychotic disorders were not further subdivided until the late 19th century.

Emil Kraepelin (1919) gave us the framework that created the modern concept of schizophrenia. One of his many great contributions was to take the general concept of psychosis and subdivide it into two major groups based on his observations of differences in course and outcome. One group of patients had an episodic course typically presenting with full remission of symptoms. A second group had a chronic course and typically progressed into a deteriorated state. He named the two groups "manic-depression" and "dementia praecox."

Kraepelin did not consider psychotic symptoms to be the most important features of dementia praecox. When he talked about the symptoms, what he considered most important would be what we call today the negative symptoms. There are passages in Kraepelin's textbook that indicate he thought negative symptoms were the most important symptoms of schizophrenia.

Bleuler (1950) on the other hand, tried to clarify the group of schizophrenias by very explicitly attempting to identify what he considered to be the underlying fundamental abnormality. As a consequence he divided the symptoms of schizophrenia into two categories: fundamental and accessory symptoms. Bleuler believed that fundamental symptoms were present in all patients, and tended to occur only in schizophrenia. The accessory symptoms on the other hand could occur in a variety of disorders. Depending on how we interpret his writings, we can argue that Bleuler identified four to six fundamental symptoms of schizophrenia. These included: the loss of continuity of associations, loss of affective responsiveness, loss of attention, loss of volition, ambivalence, and autism. These symptoms correspond somewhat closely to the current negative symptoms. In Bleuler's thinking, these symptoms reflecting abnormalities in basic cognitive and emotional processes provided the basis for other types of symptoms observed in the illness. Accessory symptoms included those such as delusions and auditory hallucinations.

When Kraepelin named the disorder "dementia praecox", he intended to highlight the fact that it had an early (praecox) onset and differed from another type of dementia described by his colleague Alois Alzheimer. However, in choosing the term "dementia", he wished to highlight the fact that the illness was chronic and deteriorating. Bleuler chose to rename the disorder to highlight his own view that a fragmenting of thinking (thought disorder) was the most important feature (as well as to eliminate the concept that deterioration was inevitable.) Bleuler's name eventually prevailed over Kraepelin's. Unfortunately, the meaning of schizophrenia, being "split mind", has many assume that schizophrenia means split personalities, but to this day no alternative has been coined.

Throughout most of the 20th century, Bleuler's perspective dominated, and clinicians all over the world were taught to define and diagnose schizophrenia based on the symptoms that Bleuler saw as fundamental.

The emphasis on negative symptoms shifted in the 1960s and 1970s. This change came primarily from an interet of improving diagnostic precision and reliability. Since delusions and hallucinations are essentially "all or nothing" phenomena, that are easy to recognize and define, they were steadily given greater prominence, being placed at the forefront of the definition of schizophrenia. This emphasis arose because of the influence of Kurt Schneider.

Schneider, like Bleuler, wanted to identify symptoms that were fundamental. This led him to discuss "first-rank" symptoms, that were characterized by loss of autonomy, such as thought insertion or delusions of being controlled by outside forces. Schneider's ideas were incorperated into many diagnostic tools. When diagnostic criteria like the RDC and DSM-III were written, they essentially ignored negative symptoms.

As the present moves towards the future, corrective adjustments are already beginning to occur. These often occur by returning to the past and coming full circle to the work of Kraepelin, Bleuler, Jackson, and Schneider, paradoxically! Clinically, the emphasis on negative symptoms as well as psychotic symptoms is leading to increased interest in the full range of symptoms of schizophrenia, and for methods for treating that full range. Complemented by the return to negative symptoms is the return to cognitive symptoms as well. Many negative symptoms are cognitive in nature, such as alogia and avolition and attentional impairment. Increasingly, investigators are returning to the original insights of Kraepelin and Bleuler that the core symptoms of schizophrenia represent a fundamental deficit in cognition and emotion.

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