Lecture 10: Psychopathology Flashcards
epidemiology of mental illness in US adults; who is most at risk
21% of adults; 4% have severe impairment
higher in females
higher in younger adults
highest in LGBTQ
racial background results in cultural factor
*drug abuse doesn’t count
most common types of mental illness
anxiety is most common = 19%
depression is next = 4%
types of mental illness
emotional - related to limbic system
- internalizing = anxiety/depression
- externalizing = drugs/conduct disorder
psychotic - more association areas involved
- i.e. bipolar or schizophrenia
**mental illness is a spectrum
examples of primary vs secondary mental illness
autism pt develops mental illness = secondary
cannabis abuse (primary) causes psychosis (secondary)
characteristics of mental illness in adolescents
most start to show in adolescence
50% of adolescents have some kind of mental illness; 11% have severe impairment
prevalence peaks at 17-18 years
no obvious difference in prevalence with sex BUT females do have different S&S than males
major increases in substance abuse in those with mental illness
how does the cerebral cortex develop/mature
matures from posterior to anterior and right to left
posterior portion of the brain is like the gas pedal (contains limbic system); everything based on emotion
anterior portion (prefrontal lobe) is like the brake; more sound/logic decision; stop impulses
L dorsolateral prefrontal cortex (last to develop) = working memory and executive functions
ratio of gray matter to white matter increases?
3 critical stages of synaptogenesis
1st: sensorimotor, 2 months before birth and peaks 1 month after
2nd: frontal, parietal, temporal association cortex; peaks around 8 months of age
3rd: prefrontal cortex develops last, peaks around 2 years of age
which critical stage is the fastest
1st/sensorimotor
fastest in utero
all 3 critical stages peak by what age
2 years
frequency of firing at peak synaptogenesis vs peak pruning
peak synpatogenesis = 4.3 million per min
peak pruning = 0.072 million per minute (lasting longer = maturation)
describe the functional connections and myelination of the brain during critical stages
whole brain has less gray matter and more white
prominent in adolescent period
males have 20% more brain mass than females; not necessarily a good thing
describe what happens to the brain with marajuana
increase in non functional connections
more connections but they are not useful and inhibit the good connections
describe the stages of brain development from 1 month to 9+months
1 month = internal capsule, projection fibers (coordination with different body parts)
2 months = long association fibers (inter regional?)
5-6 months = long association fibers (inter regional?)
7-9 months = commissure and short association fibers (regional functioning and cross talking)
over 9 months = all fibers start to mature
pathophysiology of ASD
altered functional connections
decreased long distance/subcortical connections = compromised integration functions
increased short distance association fibers (focus a lot on details but not the context of the whole situation)
core diagnostic criteria for ASD
loss of social cognition
increase of repetitive behavior
females - different S&S (more depression like)
prevalence of ASD
1-3%
prevalence of different mental illnesses secondary to ASD
10-50% = depression
80% = anxiety
30% = bipolar
28-39% = childhood onset schizophrenia
over 75% of ASD pts have one or more mental illness
what is a phenotype and what is the implication of this
universal formula
gene(s) + environmental factor(s) = phenotype(s)
some diseases are genetically predisposed; some can be managed (PKU) but some cannot (HD)
environments can promote activation or inhibition of certain genes
genetic component varies from 0-100%; decides how much of it you can manage/control
describe the types of onset of ASD
congenital = mainly prenatal and during critical development stage I (genetic/environmental)
postnatal = trauma to amygdala, temporal lobe, cerebellum, etc (environmental)
diagnosis of schizophrenia
2 of the following:
- delusion (thoughts)
- hallucinations (perception)
- disorganized speech
pathology implications of those with schizophrenia
enlarged lateral and 3rd ventricles
atrophy of frontal lobe association cortex
- frontal eye field problems; can’t smooth track
-delusion
- disinhibition function
- trouble with working memory (LDLPFC)
what S&S of schizophrenia are caused by temporal lobe atrophy
auditory hallucinations
disorganized speech; fluent aphasia/talking to the hallucination
loss of frontal temporal synchrony
loss of sensory gating (reactions are not decreased after 1st sensory stimuli is perceived)
how much of schizophrenia is genetic vs environmental
50% for both
congenital vs postnatal
congenital
- lacking nutrition
- drug abuse
- viral/bacterial infection of embryo/fetus
postnatal
- drug abuse (i.e. MJ)
- trauma to frontal/temporal lobe
types of mental illness with critical stage III
control of emotion
internalizing = depression and anxiety
externalizing = drug abuse and behavior
antisocial personality disorder = 3.5% in US
adolescents highly vulnerable to drug abuse due to brains not being fully developed yet
describe the mechanism of drug abuse and addiction
2 dopaminergic pathways initiated in middle brain
- substantia nigra/caudate and putamen = motor/cognition/emotion
- ventral tegmental/nucleus accumbens = reward seeking path
almost all addictive drugs affect the reward seeking path
what happens in the brain with binge drinking
decreases corona radiata contents (all axonal bundles of brain)
affects cognition, emotion, and behavior
compromises temporal lobe functions; 10% volume decrease in gray AND white matter
describe the negative effects of cannabis on the brain
compromises frontal lobe development
- decision making
- increases connections = false memory (emotional and psychotic mental illness)
describe the negative circuit of marajuana use
abuse = delay in prefrontal development = controls emotional development = decides future orientation = leads to more future abuse
features of depression and clinical presentation
chronic feelings of sadness and hopelessness; loss of interest in activities
clinical presentation:
- can’t accept negative feedback
- ruminating on negative results
describe the loss of functional connections with depression/ areas of the brain affected
cingulate gyrus - negative emotions
L dorsolateral prefrontal cortex - decreased inhibition function
Amygdala - decreased aversion to neg stimulus
medication management for depression
SSRIs
incidental findings
tryptophan metabolism
purpose of cognitive behavior therapy for depression
reconnection of ACC and L DLPRC
non-invasive vs invasive treatment for depression
repetitive transcranial stimulation: rTMS activates L DLPFC
deep brain stim: DBS inhibits neg circuitry
vagus n stim: balance HPA axis stress and improve alertness/arousal
what can PT do for depression pts
30 min daily high intensity exercise is better than meds and cognitive behavior therapy
describe the longitudinal impairment from early life stress and how it relates to depression
through hypothalamus pituitary gland pathway (HPA axis)
“double crush theory”
increased cortisol and sympathetic nervous system activates: sensitization
recall SNS and sleep cycle; depression is worse in winter due to decreased sunlight exposure
describe pathophysiology of HD and the implications
100% genetic predisposition
degeneration of basal nuclei and cortex (caudate is worst) = subcortical dementia
impairments of cognitive, sensorimotor, and emotional functions
prefrontal lobe injury results in what
psychopathological presentation
i.e. Phileus gage L DLPFC; compromised with psychopathology but still functional
can happen with stroke, viral infections, etc
effects fo physical activity/PT on mental illness
large effects on depression and schizophrenia
moderate effects on aerobic capacities
small effects on anthropometry
