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Trephine skull (5000 BCE)
cut circular hole out of skull to release demons
Most of early human history, psychiatric disorders were through to be supernatural (disorders due to evil spirits)
Hippocrate (400 BCE) and Galen (2nd century CE)
imbalance of body “humors” (fluids)
Believed that psychiatric disorders were due to an imbalance of internal body humors (fluids)
Breakthrough → mental disorders have a natural cause (not supernatural)
Psychopathology
the scientific study of psychiatric (mental illness and disorders)
Lunatic Asylums
solution of psychiatric disorders was to institutionalize people; lock them way and isolate them from society
St. Mary of Bethlehem (London, 1247)
earned nickname “Bedlam” after its horrific practices and conditions (state of uproar and confusion)
Pitié-Salpêtrière Hospital (Paris, 1656)
mostly for women (prostitutes, mentally ill, or just poor) prison-like conditionsand notorious for its overcrowding and inhumane treatment of patients.
Rotational Therapy
spinning people very fast to reduce “brain congestion”
Teeth removal
belief that mental illness was inflammation based
Oral and dental infections were common → removed teeth in hopes of “curing”
Benjamin Rush & Tranquilizing Chair
immobilize a person in a chair to reduce blood flow with hopes of reducing psychiatric illness
Continuous Hydrotherapy
idea that water could ease insanity if applies to the skin
Effective because water could be heated or cooled
Psychotic Disorders
schizophrenia (and many subforms), drug-induced psychosis
Affective Disorders
major depressive disorder, bipolar disorder, premenstrual dysphoric disorder, postpartum depression conditions characterized by significant mood disturbances, including periods of extreme sadness or mania.
Anxiety Disorders
generalized anxiety disorder, panic disorder, social anxiety disorder
conditions characterized by excessive fear or worry, often leading to significant distress and impairment in daily functioning.
Splitting of the mind
DOES NOT refer to multiple personalities within the same individual (dissociative personality disorder) → rather a disconnect between aspects of a single personality, thought, emotion, and behavior
psychoses
disturbances in thoughts and perceptions that result in a loss of touch with reality
Modern treatment
tends to consist of behavioral therapy and antipsychotic medicationto manage symptoms and improve functioning.
The spectrum of schizophrenia
heterogeneous set of conditions that vary widely from person to person in their severity, duration, and how they present symptoms
Positive symptoms
things that are present, but shouldn’t be
Hallucinations: false sensory perceptions
Deluations: unshakable belief something that is untrue (false belief)
Negative symptoms
things that should be present, but are not
Flattened emotions
Poverty of speech (lack of speaking)
Difficulty experiencing emotions and planning
Lack of initiative and persistence (Lack of motivation)
Isolating – social withdrawal
Anhedonia (inability to experience pleasure)
Cognitive symptoms of Schizophrenia
Difficulty sustaining attention
Low psychomotor speed
Dificenty in learning and memory
Poor abstract thinking
Poor problem solving
Difficulty with attention and applying information to make decisions (prefrontal cortex involved)
Catatonia
A complex neuropsychiatric behavioral syndrome that is characterized by abnormal posturing, immobility, and withdrawal
People are aware of their surrounding but do not interact with it
Patient may appear lifeless and exhibit posturing, muteness, staring, and immobility
age of onset schizophrenia
20.5 is average but late 20s early 30s for women
schizophrenia prevalence
1-1.5% of the us population (3 million ppl)
genetic basis of schizophrenia
Risk of development increase with number of genes shared by a family member with the condition
General population has a 1% lifetime risk
50% shared genes with parents puts you at a 6% risk of developing
Monozygotic twins have 100% of the same genetic makeup but only puts the twin at a 48% risk of development
environmental factors of schizophrenia
People who develop schizophrenia without a family history often experienced more complications at birth (compared to neurotypicals):
Ex. low birth weight, prolonged labor
Can also be related to to the mothers health at time of fetal development
hunger winter ww11
Food was scarce, causing mothers to be malnourished → this resulted in a large number of the offspring to develop schizophrenia (compared to the normal population)
Seasonal effects schizophrenia
higher number of schizophrenic births during winter months
If mother becomes ill (e.g. flu) during the 2nd trimester, the offspring is more at risk to develop schizophrenia
Mothers body is fighting infections → Could lead to inflammation which is detrimental to fetal development
adolescent behavioral deficits linked to schizophrenia
motor abnormalities, apathy, social withdrawal, attention deficits, etc.
Symptoms are hard to spot and often go misdiagnosed (assumed to be autism)
Irrespective of whether the parent is ‘normal’ or schizophrenic
Cortical gray matter loss
“cerebral atrophy”) – excessive synaptic pruning in the perinatal and adolescent periods
Cerebral atrophy (within/ death of cortical neurons) is normal in early development → we are born with more than we need and are progressively pruned
Strong connections survive and integrate with the brain white weak ones die off
HOWEVER pruning happens at abnormal (accelerated) rates to people with schizophrenia → they experience ~2x greater cortical neuron loss
Ventricular enlargement following gray matter loss
Ventricles which hold cerebrospinal fluid are enlarged → likely because the significant loss of gray matter allows for more room for the ventricles to expand (less brain tissue around it)
Disorganised hippocampus cytoarchitecture (neuron migration issues in development)
In neurotypical individuals hippocampal neurons have an orderly arrangement – lined up in an organized manner
Schizophrenic individuals – there is a lack of arrangement (disorganization) → this can lead to neural connectivity issues
Neurons have trouble making the right connections because they are in the wrong places → making more synaptic connections is more difficult because neurons are not in the right positions
Indicates neurodevelopmental abnormalities in neuron formation, mitigation, and synaptogenesis
Shrinking of dendritic trees leading to connectivity failures (issues with synaptogenesis)
Shrinking of dendritic spines, usually in cortical neurons → abnormally small which suggests fewer synaptic connections
Related to issues in making new synaptic connections (synaptogenesis)
two-hit model
biopsychosocial interactions that show two developmental points of schizophrenia in time
early stage “first hit”
Perinatal Period
Genetic predispositions and gene expression + Environmental insults (virus,toxins, poor nutrition, birth complications, activated immune system)
Result → neurodevelopmental abnormalities from conception to early adulthood including neuron formation, mitigation, synaptogenesis, pruning, apoptosis
Latent Stage
First Few Years of Life:
Early subtle signs of prediction schizophrenia including motor abnormalities, apathy, social withdrawal, deficits in attentional and information-processing tasks
Late Stage “Second Hit”
Adolescents
Excessive synaptic pruning in adolescence leading to abnormal neural connectivity and function + later environmental insults such as stress, substance use, and HPA axis dysfunction
Greater impairment of cognitive function including deficits in attention, memory, executive function
Positive symptoms including hallucinations, delusions, disorganization
Worsening of negative symptoms include deficits in motivation and emotion, isolation, anhedonia
Neurodevelopment/Hypofrontality Hypothesis
here are defects in early brain development (particularly in the frontal cortex) → results in reduced PFC activity
Believe that cognitive symptoms seem PFC dependent
The frontal cortex is less active (hypoactivity) in individuals with schizophrenia
Ex. give an executive function task to an individual believed to have schizophrenia (while in a scanner) → if they have the condition, we will see low prefrontal cortex
Lack of activity likely reflects lack of glutamatergic neurons
The Dopamine Hypothesis
Schizophrenia is due to hyperactivity of dopamine circuitry (too much DA signaling)
Evidence: drugs that enhance DA activity can produce positive symptoms of schizophrenia
Ex. amphetamine psychosis → chronic heavy use can produce positive schizophrenia symptoms
Causes psychotic episodes and feeling like ants are crawling on you skin (hallucinations)
Results because of an access of dopamine activity
The first effective antipsychotic drugs are antagonists of dopamine “D2” receptors (inhibits activity)
HOWEVER if schizophrenia were due to a simple overabundance of dopamine, antipsychotics would work immediately → BUT they usually take several weeks to take effect
This suggests more complex mechanism
AND the negative and cognitive symptoms usually DO NOT improve with D2R blockade
The Glutamate Hypothesis
Schizophrenia is due to hypoactivation of glutamate circuits (too litter GLU signaling)
Evidence: drugs that mimic some symptoms of schizophrenia are glutamate receptor antagonists
Ex. PCP and Ketamine can create detachment and hallucinations
