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64 Cards in this Set

  • Front
  • Back
In schizophrenia the brain undergoes
volume reduction and laterla and third ventricular spaces are larger.
schizophrenia is characterized by
mixture of positive, negative, cognitive and mood symptoms
Onset of schizophrenia is
usually during adolescence or early adulthood; age of onset is earlier in males
The only effective schizophrenia treatment is
Dopamine 2 antagonist (antipsychotics) are the only effective therapeutic agents, which are currently available
§ It is often marked by
diminished drive and emotion during childhood , followed by a break in self-monitoring abilities which results in perceptions and/or ideations that deviate substantially from the individual's cultural norm, which is usually expressed as false beliefs, auditory verbal hallucinations and abnormalities of thought / language.
19. Schizophrenia presents with
a. Positive symptom vs. negative symptom
i. Positive symptoms
hallucinations, delusions, disorganized behavior and speech
ii. Negative symptoms
avolition, anhedonia, flat affect
iii. Drugs only help positive symptoms
Schizophrenia, psychosis usually emerges between
age 17 and 30 in males and age 20 and 40 in females, with the course and outcome that varies considerably between individuals.
Most Schizophrenia patients, however, do improve from the initial episode
continue to manifest some symptoms, and remain vulnerable to periodic exacerbation of psychotic symptoms.
In general, while the severity of psychosis plateaus within 5 to 10 years of the first episode, but
diminish drive and emotion may worsen over a longer period.
Schizophrenia late in life there is a tendency toward
decreased intensity of symptoms and some improvement of function, this does not compensate for years of lost experience and opportunity.
b. Phases of schizophrenia
i. goes from premorbid → prodromal → onset deterioration → chronic/residual
ii. As you age, you get better (less episodes)
besides positive and negative symptoms what else is needed to diagnose SZ?
-Decline in role functioning, self-care
-Minimum 6 months of symptoms
Brain volume changes in
first-episode schizophrenia
The Development of Chlorpromazine
Derived from methylene blue dye is the only one that seems to improve patients conditions
Recent large-scale studies like CATIE suggest 1st v. 2nd generation of antupsychotics distinctions probably less true due
to dosing issues
Cognitive enhancement” of new drugs may just be due to
switching treatment refractory patients to the newer drug, thus “releasing” them from an old drug that given at a high dose and may have interfered with cognition
Although cognitive dysfunction is SZ is not a diagnostic feat it is important for treatment development because
Correlation of cognitive dysfunction to poor outcome § Lack of current effective treatments for poor cognition
• No antipsychotic helps cognitive function improve
• “cognitive enhancing” (dementia drugs) do not help • Important for providing information about underlying
neuropathology of schizophrenia
Pathogenesis of SZ may include
-genetic components
-cellular programming
-cell development
-neural systems
-behavioral functions
Genes components contributing to sz
Multiple susceptibility alleles each of small effect
Neural systems related to sz
Abnormal connectivity in local and associational circuits
Behavioral functions related to SZ
Disturbances in perception, information, processing, mood regulation, cognition
SZ Genetic component in twins are highly correlated
1. 50% concordance with monozygotic twins
2. 1st degree relatives without dx of SZ show many of the same traits
Enviromental components related to SZ
1. people in high expressed emotion households are at risk, and high marijuana users
2. prenatal events like mother having flu, rubella, pre-eclampsia, STD at time of conception..
The absence of a clear phenotypic distinction across diverse psychotic states such as schizophrenia, psychotic affective disorder and schizophrenia has led to one view that these disorders might represent
a continuum termed the Unitary Psychosis Model.
Alterations in attention and information processing in schizophrenia have been thought to result from a failure of
filter mechanisms leading to schizophrenia related psychopathology
Frith and Done (1988) originally proposed that symptoms of alien control (i.e. first rank symptoms) in schizophrenia might result from
problems with the central monitoring of responses.
Crow (2000) has proposed that nuclear symptoms of schizophrenia may be related to
a disintegration of language processes that is uniquely human and emerges in the context of speciation.
Kapur (2003) proposed that psychosis may result from an aberrant assignment of salience to the elements of
one's experience as a result of dopaminergic dysregulation.
none of the Models of Phenotypic Expression explains
the broad body of the “facts of schizophrenia”.
Schzisophrenic people have a delusion of control they feel someone of is controlling their movements, they show
contralateral motor and sensory activaition as if in fact someone was controlling their movemebts
Observations of alterations in synchronous oscillations in the gamma range (30–80 Hz) have led to the theory that psychopathology in schizophrenia may result from
dysfunction of inhibitory circuits
e. Corollary discharge – an explanation of hallucination
i. Corollary is sending copy of instructions to other sensory regions of the body to cancel stimulation: hallucination is when these systems go awry
ii. Efference copy is an internal copy created with a motor command of its predicted movement and its resulting sensations. One role of efference copies is to enable the brain to estimate the sensory feedback from movements in which case they are called corollary discharges.
It should be noted that a white matter disease such as metachromatic leukodystrophy can mimic schizophrenia with its
psychosis phenotype
The widely held neurochemical hypothesis, the classic hyperdopaminergic model has in recent years given way to more complex and integrative views such
as the prefrontal–limbic dopamine (DA) imbalance model and the phasic–tonic DA imbalance model
Dopaminergic models are strongly supported by the fact that all currently available antipsychotics work by
blocking dopaminergic receptors, and also by clinical observations of psychotic symptoms in individuals following repeated amphetamine use.
DA blockade may be a necessary and sufficient explanation for antipsychotic effects (Kapur and Mamo, 2003), and by inference, to
the positive symptom dimension of schizophrenia.
DA imbalance models provide an integrative view of
cognitive and negative symptoms with psychotic episodes, though not other aspects of the illness such as structural alterations and functional decline.
Amphetamine-induced sensitized state has been used as an animal model for some domains such as
symptoms, but not other domains such as negative symptoms
DA related genes do not appear to explain the substantive heritability of schizophrenia, and dopaminergic treatments
have little effect of cognitive and negative symptoms.
t is quite likely that DA alterations are involved downstream in the final common pathways that lead to psychosis (Seeman, 2010), though the primary causal events
remain elusive.
Alteration in the excitatory neurotransmitter glutamate system, especially involving N-methyl-d-aspartate (NMDA) receptor function has emerged as a promising
pathophysiological model.
NMDA receptor model stemmed from
early observations that phencyclidine (PCP) causes symptoms closely resembling schizophrenia. Early age pcp doesn't causes psychotic effect only in later life..similar to the onset of the disease
Glutamatergic constructs such as the NMDA receptor hypofunction model have considerable explanatory power:
ntegrates the early and late developmental deviations
§ The role of dopamine
§ The post-illness onset deteriorative processes that occur in schizophrenia.
Many genes implicated in schizophrenia appear to converge on the
glutamatergic system. However, this model does not clarify why, despite the ubiquity of glutamatergic neurons in the brain, schizophrenia is not associated with more generalized neurological impairment
Medications that modulate the glycine site of the NMDA receptors have been reported to
improve cognitive deficits in schizophrenia.
Several lines of evidence indicate that gamma amino acid butyric acid (GABA) neurotransmission, the main inhibitory neurochemical system, is dysfunctional in schizophrenia.
§ Post-mortem studies have consistently reported reductions in
GABA neurons and/or key enzymes related to this pathway.
It has been suggested that observations of altered neural synchrony and cognitive deficits in schizophrenia may be related to
altered GABA neurotransmission.
The membrane hypothesis posits the role of
membrane alterations in peripheral cells as well as the brain
The membrane hypothesis is appealing since membranes are critical for
several aspects of neuronal function such as receptors, channels and signal transduction.
The inflammation hypothesis of schizophrenia is based on observations that schizophrenia may be associated with
an increased serum concentration of several pro-inflammatory cytokines that may reflect response by microglia to various pathological processes in the brain
The pathophysiology of schizophrenia has also been thought be related to increased oxidative stress (accumulation of reactive oxygen species that may damage neuronal function) in this illness, supported by
observations of decreased antioxidant and increased pro-oxidant processes
The “early” developmental models suggest that disruptions in intrauterine or early postnatal life, i.e. neuronal proliferation, migration, differentiation and elimination, or neurogenesis processes, may lead to
impaired neural infrastructure and abnormal brain maturation predisposing to premorbid dysfunction as well as psychopathology emerging later in adolescence or early adulthood.
The “late” developmental models, which account for the typical onset of schizophrenia during adolescence, propose
deviations in later emerging processes such as synaptic/axonal pruning or neuronal apoptosis and/or myelination processes contribute to its evolution.
It has been known for long that schizophrenia is highly heritable.
§ The most promising etiological models therefore include the view that
schizophrenia may be polygenic/multifactorial.
Though recent linkage and genome-wide association studies have identified a large number of candidate genes and specific risk alleles for schizophrenia, replicated findings explain only
a very small fraction of the heritability.
The view that schizophrenia may be caused by multiple common genes each conferring a small effect has been supported by
genome-wide association studies (GWAS). These alleles present relatively modest odds ratios (the odds of a risk variant being present in cases vs. controls) and suggest causal roles of gene regulatory mechanisms in Schizophrenia.
In recent years, observations have emerged of rare and unique mutations and copy number variations (CNV) conferring
possibly severe risks seen in a significant proportion of patients, though no single locus explains more than approximately 1% of cases.
he relationships between genes (e.g. DISC1, neuregulin) and their neuropathological consequences (such as dendritic morphology) are not straightforward, and are likely to be influenced by
profound gene–gene and gene–protein interactions, leading to incredibly complex “interactomes”.
Gene–environmental models suggest that interactive effects of genes and environment on biological pathways may have
larger effects than either genes or environment.
A large fraction of the heritability of schizophrenia may be accounted for
by gene–environment interaction.
An integrative approach is the “two-hit hypothesis” which proposes that genetic risk and early developmental alterations (first hit) may
prime the person to react to a second hit in the form of an environmental factor later during development leading to the illness.
n epigenetic model, which is increasingly gaining recognition, posits that environmental factors impact on gene expression via changes in
DNA methylation and chromatin structure which, in turn, may play a role in the etiology of schizophrenia.