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90 Cards in this Set

  • Front
  • Back
dopamine synthesis locations
midbrain, corpus straitum, pars compacta, VTA
Serotonin low levels
depression, OCD, Panic, and Bulimia
Serotonin high levels
Anxiety, insomnia, sexual dysfunction, GI disturbance, serotonin sydrome, cardiac valce pathology
Serotonin syndrome
fever, tremor, coma, seizures, death
dopamine secreting cells
some make also NE
NE
attention, motivation, pleasure, reward
DA
Alertness and energy
5-HT
Obsessions and compulsions
Mood
NE, DA, and 5-HT
Anxiety
DA and 5-HT
D2 and D4
inhibitory
D1
excitatory
NE levels
same for all of us, receptors are variable
NO
retrograde messenger
NO drugs
Viagra and sunadafil increase levels
NO synthesis
at post-synaptic neuron
NO purpose
feedback process, down regulate
Brain disorder pathology
start early in life, need a lot of damage for clinical symptoms
Epilepsy
having two or more seizures
Epilepsy tests
EEG and brain scan
Epilepsy cause
sustained repetitive firing of APs
Epilepsy factors
genetic and acquired, cerebral trauma, infx, tumor, congenital malformation, metabolic
Epilepsy focal
within one area, majority of patients
Epilepsy generalized
All over the brain
Epilepsy brain sites
areas susceptible to attacks
Temporal lobe epilepsy
most common form of dz, dentate gyrus initiates seizure
Voxel-based morphometry
allows investigation of focal differences in brain anatomy
Temporal lobe epilepsy, VBM
hippocampal atrophy with seizures originating in left or right lobe
Epileptogenesis
excessive excitation or reduced inhibition, or channelopathy
SUDEP
Sudden Unexpected Death in Epilepsy
SUDEP occurance
more likely if seizures are more frequent or tx is inadequate
SUDEP most cases
from a Grand Mal Seizure
SUDEP cause
apnea or asystole
Schizophrenia symptoms
positive, negative, and cognitive
Schizophrenia positive symptoms
hallucinations, delusions, racing thoughts
Schizophrenia negative symptoms
apathy, lack of emotion, poor or nonexistant social functioning
Schizophrenia cognitive symptoms
disorganized thoughts, difficulty concentrating and/or following instructions, difficulty completing tasks, memory problems
Schizophrenia theory
caused by development and plasticiy disorder with risk genes
Risk genes
dysbinidin, neuroregulin 1, DISC1, COMT
Dysbindin
dystrobrevin-binding protein 1, is a protein constituent of the dystrophin-associated protein complex
DISC1
disruptive in schizophrenia gene, participates in cell growth, movement, axonal growth and transport, neural positioning.
COMT
Catechol-O-methyl transferase, degrade catecholamines such as dopamine, epinephrine, and norepinephrine
neuregulin 1
heightened expression of the Type IV NRG1
Schizophrenia and ventricles
enlarged lateral ventricles, empendymal or spiny cells lost
Schizophrenia etiology
Epigenetic dysfunction, Risk gens, rubella, influenza, herpes, toxoplasma gondii, hypoxia, malnutrition, OB complication, premature/low birth weight, preclampsia, and C-section
Toxoplasma gondii
from cats, can cross placenta
ADHD
a neurodevelopmental problem
ADHD presentaion
age-inappropriate symptoms of inattention,impulsivity and hyperactivity
ADHD brain abnormalities
frontal and temporal lobes and basal ganglia
ADHD neurobiology
hypoactive frontal-striatal region due to deficient DA transmission
Depression symptoms/signs
anhedonia, vague aches and pains, insomnia or hypersomina, weight loss/gain, low energy and fatigue, and recurrent thought of death/suicide
Dysthymia
depressed all the time
Psychotic depression
delusions, beliefs, and feelings that are untrue/unsupported. Bipolar may experience during depressed state
Reactive depression
adjustment disorder with depressed mood response to a psychosocial stressor
Atypical depression
able to experience improved mood via a positive event
Melancholic depression
inability to find pleasure in a positive things, combined with physical agitation, insomnia, or a decreased appetite
Depression etiology
genetics, emotional trauma and viral infx, stress(HPA axis) and cytokines, and signaling pathways that regulate neuro-plasticity
Neuroplasticity
changes that occur in the organization of the brain as a result of experience
HPA axis and depression
high levels of cortisol cause depression
Subventricular zone
neurogenesis, olfactory
Subgranular zone
neurogenesis hippocampus
Seasonal affective disorders
imbalance between sleep/wake cylce and brain cycle
Seasonal affective disorders etiology
dysregulation of 5-HT transmission and mutations
TPH2
rate limiting enzyme, 80% reduction in enzymatic activity if mutated
hTPH2
loss-of-f(x) mutation, seen in unipolar depression
treatment resistant depression
common occurrence
OCD etiology
rouge genes, head injury, autoimmune reaction
Sydenham's chorea
suffer from antibodies for Gram + bacteria, and show disorders of hand face feet. Treated with antibiotics
PANDAS
Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus
Sydenham's chorea antibodies
against strep and attack neurons of caudate nucleus
Molecular mimicry
same biochemical sign as illness and body attack both exogenous agent and own self
Molecular mimicry example
SLE and NMDA receptors
Tourette Syndrome presentation
multiple tics and one or more vocal tics
GTS causes
childhood tics
GTS population
more common in males than females
GTS etiology
genetic, Panda, other viral
Simple GTS
motor and vocal tics
Full Blown GTS
coprolalia, copropraxia, echolalia, echopraxia
coprolalia
obscene/vulgar sounds
corpropraxia
obscene/vulgar movements
echolalia
imitation of sounds
echopraxia
imitation of movements
Polyglutamate pathogenesis
nine neurodegenerative disorders by expanding CAG repeats
Huntington Pathology
striatal cell die, motor cortex becomes hyperactive
Huntingons mutation
huntingtin on end of chromosome 4, Autosomal dominant
CAG repeats normal
10-29, and a few tieh 30--35
CAG repeats in HD
40-60
HD appearance
atrophy of caudate nucleus, putamne, hydrocephalus ex vacuo (anterior horns)
HD slide
GFAP shows gliosis
HD protein
mutant protein aggregates and is toxic to neurons