Biological Bases of Behaviour Flashcards
central nervous system
spinal cord
+
brain (which includes the cerebrum, cerebellum, and brain stem)
peripheral nervous system
somatic nervous system
+
autonomic nervous system (which includes the sympathetic nervous system and the parasympathetic nervous system)
somatic nervous system
sends and receives messages that control voluntary motor movements of the skeletal muscles
autonomic nervous system
controls automatic or involuntary bodily functions of the smooth muscles and glands (digestion, heart rate, breathing)
sympathetic nervous system
the “mobilizing” system, dominant during times of stress, controls the fight or flight response
parasympathetic nervous system
the “energy conserving” system, dominant when a person is relaxed
quadriplegia
- severing of the spinal cord anywhere between C1 and C5
- all 4 limbs are paralyzed
paraplegia
- severing of the spinal cord at C6 or C7 = paralyzed legs and partial paralysis in arms
- severing of the spinal cord at T1 or below = paralyzed legs only
paresis
- incomplete severing of the spinal cord
- results in muscle weakness
left hemisphere
- dominant in about 97% of people
- responsible for rational, analytical, logical, and abstract thinking
- damage can result in aphasia, language problems, apraxia, and difficulties with the right side of the body
- positive emotions (L for love)
right hemisphere
- responsible for perceptual, visuospatial, artistic, musical, and intuitive activities
- damage can result in left-side hemi-neglect, prosopagnosia, visual perceptual disturbances, impulsivity, abnormal sexual behaviour
- negative emotions (think what does music help regulate?)
Broca’s aphasia
- located in left frontal lobe
- controls muscles that produce speech
- damage results in an inability to express language
- speech is slow and effortful (short phrases and lengthy pauses)
Wernicke’s aphasia
- located in the left temporal lobe
- involved in verbal memory and language comprehension
- damage results in an inability to comprehend speech
- fluent spoken language but sentences are nonsensical
conduction aphasia
- intact language comprehension, fluent speech but nonsensical
- cannot repeat verbal phrases
- can follow through with verbal commands because comprehension in not impaired (unlike Wernicke’s), no slowed speech like in Broca’s
global aphasia
- most language functions are impaired (fluency, comprehension, repetition, naming)
parietal lobes (gertmans syndrome)
- processes somatosensory information (shape, size, weight, texture, pain, heat, movement of the body) bc somatosensory cortex is here
- damage causes: asomatognosia (not aware of body parts), Anosognosia (denial of illness), hemispacial neglect(contra lateral neglect; neglect one’s side of body ie. dress only one side of body), ideomotor apraxia (can’t carry our movements if told to do something) , ideational apraxia (can’t conceptualize sequences or steps involved in movements) AND Gretsmann syndrome (left parietal lobe damage, agraphia, acalculia, right left finger agnosia and disorientation)
proprioception
ability to sense position, location, and movement of the body
frontal lobes
- largest portion of the brain
- Broca’s area is here.
- 3 main divisions = prefrontal cortex, premotor area, motor area
- critical to personality, emotionality, inhibition, planning and initiative, abstract thinking, judgment, and higher mental functions
- damage can result in loss of movement of various body parts, changes in personality, emotional lability, perseveration, inattention, difficulty with problem-solving, Broca’s aphasia. DOESNT impact IQ (bc damage only impacts divergent thinking NOT convergent thinking which IQ tests measure)
occipital lobes
- involved in sight, reading, and visual images
- damage can result in difficulty recognizing drawn objects, and achromatopsia (difficulty seeing colours/identifying colours, visual agnosia (hallucinations and illusions), and inability to recognize words / problems with reading or writing, prosopagnosia (inability to recognize familiar faces), cortical blindness (loss of vision)
- research: some people with cortical blindness experience blindsight= not consciously see things but reach for it or can feel/identify sad feeling when presented by a sad picture without seeing it (affective blindsight)
temporal lobes
- contains the primary auditory cortex
- also involved in emotional memory and behaviour
- damage can result in increased aggression, increase or decrease in sexual behaviour, problems with declarative memory, Wernicke’s aphasia also auditory agnosia (inability to recognize familiar sound).
corpus callosum
bundle of nerve fibres that serve as a bridge between the left and right hemispheres making it possible for the two to communicate
split-brain patients
- severed corpus callosum
- information cannot be shared with or transferred to the opposite hemisphere of the brain
- dichtonic listening task (language lateralization)
thalamus
- sensory relay center
- receives input from all senses (except smell), then processes and integrates it before projecting it to the appropriate other areas of the brain
hypothalamus
- major role in homeostasis
- regulates temperature, hunger, thirst, sex, cyclic sex hormone secretion, aggression, the sleep-wake cycle and involved in pituitary gland stimulation (important for oxytocin release)
- electrical stimulation: trouble regulating emotions
- mammillary bodies is in SCN (body’s biological clock) and that’s in the hypothalamus
- research: initiates development of secondary sex characteristics, also involved in release of oxytocin for childbirth and milk release and baby bonding. Women also react to stress with an oxytocin release which supports initiation/maintenance of relationships
Kluver-Bucy syndrome
- first described in monkeys that had their amygdala’s removed
- results in placidity, apathy, hypersexuality, hyperphagia (overeating), and agnosias (problems with recognition), psychic blindness
septal rage syndrome
can be a result of damage to the septum (which moderates and or decreases aggression)
cerebellum
- responsible for maintaining smooth movement and coordinating motor activity
- controls the automatic adjustments of posture and muscle tone that allow us to maintain balance and equilibrium
- damage: ataxia (drunk), nystagmus (jerky eye movements)
pons & medulla
- involved in sleep, respiration, movement, and cardiovascular activity
- damage can lead to failure of bodily functions and death
- pons: connector and relays messages between cerebellum and cortex. Connects 2 halves of cerebellum and helps to coordinate movements on 2 sides.
- medulla: BP, swallowing, heart rate and breathing
reticular activating system (RAS)
involved in the sleep-wake cycle, serves as a filler for incoming sensory information, and mediates alertness
all or none law
a neuron, if sufficiently stimulated, will fire to it’s fullest extent… if it is not sufficiently stimulated, it will not fire at all
inhibitory neurotransmitters
- decrease the likelihood of an action potential
- GABA, endorphins, serotonin
excitatory neurotransmitters
- increase the likelihood of an action potential
action potential
- involved in cell-to-cell communication
- how it works: when dendrites receive sufficient stimulation.. depolarization occurs as positive charged ions (NA+) enter neuron. When stimulation reaches minimum threshold, complete depolarization occurs and it triggers action potential. After this, neuron returns to resting state.
- sodium (Na+) outside of the cell membrane rushes into a cell, creating an action potential (electrochemical impulse)
- potassium (K+) moves outside the cell
agonists
enhances the effect of a neurotransmitter
antagonist
inhibits the effect of a neurotransmitter
acetylcholine
- two significant functions = voluntary movement and memory/cognition
- role in parasympathetic system
*Alzheimers (depletion of ach)
catecholamines
dopamine + norepinephrine
role of dopamine in schizophrenia
- psychotic symptoms are a result of an excessive amount of dopamine or hyperactivity of the dopaminergic receptors
- revised dopamine hypothesis: hypersecretion of dopamine -> positive symptoms, hyposecretion-> negative symptoms
role of dopamine in Parkinsons
- tied to a decrease in the dopamine available in substantia nigra & basal ganglia
- treatment = L-Dopa or Levadopa
dopamine
- involved in personality, mood, sleep, thought/memory, movement, and emotion
- reward system of the brain
*linked to Tourette & Parkinson’s
norepinephrine
- significantly involved in mood, attention, dreaming, learning and certain autonomic functions
- also involved in pain perception and sleep
serotonin
- significantly involved in mood, sleep, appetite, aggression, sexual activity, temperature regulation, arousal, aggression, and pain perception
*migraines, schizophrenia (high serotonin), anorexia
role of serotonin and norepinephrine in depression
- deficiency in both
role of serotonin and norepinephrine in mania
- low serotonin, excess norepinephrine
role of GABA in anxiety
insufficient levels of GABA
hypothyroidism
- unexplained weight gain
- sluggishness
- fatigue
- impaired memory / intellectual functioning
- sensitivity to cold
*sometimes mimics depression
hyperthyroidism
- weight loss despite increased appetite
- heat sensitivity
- sweating
- diarrhea
- tremor / palpitations
- fatigue
- agitated depression
- insomnia
- impaired memory / judgment
- hallucinations / delusions
*sometimes mimics anxiety or manic episodes
corticosteroids
involves in the use of energy resources, inhibition of antibody formation, and inflammation
Addison’s disease
- undersecretion of corticosteroids or adrenal insufficiency
- symptoms = apathy, weakness, irritability, depression, gastrointestinal disturbance
Cushing’s disease
- oversecretion of corticosteroids
- symptoms = agitated depression, irritability and emotional lability, difficulties with memory and concentration, suicide, swelling of the face/neck/trunk
neurocognitive disorder (RECSPL)
a decline in ONE OR MORE of 6 cognitive domains:
- complex attention
- executive function
- learning and memory
- receptive language
- perceptual-motor
- social cognition
mild vs. major neurocognitive disorders
- the distinction is based on the extent to which the cognitives symptoms interfere with daily functioning (how many domains or which domains are effected do not play a role)
- if they interfere with independence in everyday activities = major
- if they don’t interfere with independence in everyday activities = minor
delerium
- a disturbance in attention and awareness
- onset is rapid and course tends to fluctuate
- only diagnosed when symptoms have a physiological cause
- reversible (unlike neurocognitive disorders)
Alzheimer’s
- most common neurocognitive disorder (60-80% of cases)
- symptom progression: memory, language, motor skills
- first symptoms = short term memory loss, anomia, loss of spontaneity, depression/anxiety (2-4yrs)
- progressive disease = anterograde/retrograde amnesia, hallucinations, sundowning, flat/liable mood, restless/agitation, sleep/language troubles (2-10yrs)
- final stage of disease = severe cog functioning, urinary/fecal incontinence, loss of basic motor skills and self care skills, abnormal reflexes, seizures and frequent infections
- high glutamate, low Ach in enthorial cortex/hippocampus
- amyloid plaques(beta amyloid), intracellular neurofibrillary tangles (tau). First signs in locus caeruleous, high risk for Down syndrome.
-Big 5= low concienciousness and high neuroticism - diagnosis: only can be confirmed by autopsy, brain biopsy. Can use molecular imaging, CF fluid protein test, CT/MRI, mental status exam, neuropsych testing.
vascular neurocognitive disorder
- second most common neurocognitive disorder
- first symptoms = impaired judgment / inability to make plans
- onset is usually younger than Alzheimer’s
- typically die within 2-3 years
- stepwise progression
Huntington’s disease (chorea, globe)
- fatal disease
- involuntary movements
- also known as chorea
- early symptoms = irritability, apathy, disinhibition (emotional symptoms)
- progressively deteriorating major NCD
- choreiform movements (frequent, discrete, brisk jerking movements) and athetosis (slow writhing movements), facial grimaces
- caused by autosomal dominant gene
- linked to GABA (low), glutamate (high), dopamine in the basal ganglia and Ach (low)
-degeneration in globus pallidus - it’s a form of subcortical dementia so it wouldn’t include apraxia, aphasia or agnosia* (which do occur in Alzheimer’s)
concussion vs. contusion
concussion = not hard enough to cause a cerebral contusion
contusion = bruising and bleeding of the brain
post-concussion syndrome
- headache, dizziness, irritability, anxiety, insomnia, hypochondriacal concern, hypersensitivity to noise, hypersensitivity to light, fatigue
open head injuries
penetration of the skull
closed head injuries
the skull is not pierced or cracked
pseudodementia vs. NCD
pseudodementia = people complain about symptoms more and symptoms are relieved once depression is treated
NCD = people lack insight to symptoms and symptoms cannot be relieved
Korsakoff’s syndrome
- common cause of alcohol-induced NCD
- results from a chronic thiamine deficiency
- retrograde amnesia and confabulation are common symptoms
- lack of insight, limited spontaneous conversation, problems with executive functioning, disorientation, apathy, and labile irritability
- short-term memory remains intact**
retrograde amnesia
- you can’t recall memories that were formed before the event that caused the amnesia.
- recent memories typically more affected than remote memories from yrs ago
anterograde amnesia
- the loss of the ability to form new memories after accident
- information does not transfer from short-term memory to long-term memory
effects of bilateral vs. unilateral ECT
- bilateral causes greater memory impairment than unilateral
- some believe unilateral is less effective but if the dose of electricity is adequate it can be equally effective
gate control theory of pain
- neural gates in the spinal cord allow pain signals to continue to the brain… pressure stimulation closes the gates (this is why rubbing a hurt area can relieve pain)
- attitude/mood can affect the gates as well
stages of sleep (BATSDR)
Stage 1 - theta waves
Stage 2 - sleep spindles, K complex
Stage 3 & 4 - delta waves /deep sleep
Stage 5 - REM
*beta waves = be alert
*alpha waves = ahhh relax
OA= sleep advance, sleep latency or REM decreases as you get older BUT you still get about the same amount of REM sleep throughout life. Just spend less time in stage 3/4 sleep and REM and spend more time in stage 1/2 (lighter stages of sleep), have lucid dreaming in stage 1
generalized seizures vs. partial seizures
- generalized = affect the entire brain
- partial = limited to one specific of one cerebral hemisphere
tonic clonic vs. absence seizures
(generalized)
- tonic clonic (grand mal, loss of consciousness, stiff muscles, jerking movements)
- absence (petit mal, change in level of consciousness, between 0-30 seconds, blank stare or rolling eyes, continue on after as if nothing happened with whatever they were doing before! Looks like daydreaming. Common in kids)
PET/SPECT scans
radioactive material injected into vein, inhaled, or swallowed - measures blood flow to detect abnormalities
MRI/fMRI/MR spectroscopy
measure blood flow in brain during specific task, can determine diseases
CT scan
shows brain structure
positive symptoms of schizophrenia
- hallucinations
- delusions
- disorganized thinking
- positive symptoms tied to excess dopamine
negative symptoms of schizophrenia
- flat affect
- lack of motivation
- poverty of speech
- Negative symptoms (like lack of motivation) and cognitive issues involve glutamate and low levels of dopamine. Serotonin’s role is less clear, but its believed to affect mood.
side effects of antipsychotics
- sedation, drowsiness, dizziness, weight gain, sexual dysfunction
- anticholinergic and extrapyramidal symptoms
mechanism of action for 1st gen antipsychotics & 2nd Gen antipsychotics
- 1st Gen: dopamine D2 antagonists (positive)
- 2nd Gen: dopamine & serotonin antagonists or inverse agonists that decrease effects of dopamine and serotonin (positive & negative)
anticholinergic effects
dry mouth, constipation, urinary retention, blurred vision, dry eyes, photophobia, nasal congestion, confusion, decreased memory
extrapyramidal symptoms (DAPT + brady)
These symptoms are caused by decreased dopamine and increased ach in the nigrostriatal pathway
- dystonia or acute dystonia (occurs quickly, within hrs/days, looks like painful muscle spasms in face/neck/throat, often can’t open eyes and mouth is wide open/can’t close it)
- akathisia (takes days/weeks to develop, looks like extreme restlessness, inability to sit still, jitteriness, associated with premature termination of treatment)
- Parkinsonism (if taken for a few months this can occur, looks like Parkinson’s so tremors, muscle rigidity, mask like face, drooling, shuffling gait)
- tardive dyskinesia (taken for 6+months this can occur, looks like repetitive muscle contraction particularly in the mouth &jaw, more common in W and OA). Ok to gradually withdraw, 50% experience full remission.
- Bradykinesia: slowing down of spontaneous movement which may appear as decrease in facial expressions (symptom of Parkinsonism)
tardive dyskinesia (what is it, who is it more common for, how to treat)
- abnormal movements of the lips, tongue, and jaw
- may involve the trunk and arms as well
- not dangerous but adds to the stigma. Irreversible sometimes.
- more common in older adult and women ***
- treatment: gradual withdrawal admin a BENZO or switch to 2nd Gen antipsychotic
agranulocytosis
- potentially lethal
- sudden drop in white blood cell count
TCAs vs. MAOIs vs. SSRIs vs. NDRI vs. SNRI
- SSRIs = generally well tolerated, few side effects, minimal lethality, safer for OAs, less cardio toxic than TCA
- SNRI = more efficacious than SSRI at severe depression, neuropathic pain here too (same as TCA)
- TCAs = cardiotoxic, can be lethal if taken in overdose. Secondary (nortriptyline, desipramine) have fewer side effects. Good for neuropathic pain too.
- MAOIs = oldest class of antidepressants, highly effective for atypical depression/treatment resistant, interact dangerously with certain foods/medications
- NDRI: doesn’t cause sexual dysfunction, few anticholinergic effects and not cardiotoxic. NOT good for insomnia/anxious patients bc of energizing effect (norepinephrine). But GOOD: low motivation/energy bc of it.
mechanism of action for antidepressants
- block reuptake of serotonin or norepinephrine (increasing them in the brain)
mechanism of action for benzos
enhance the effects of GABA
withdrawal from alcohol and benzos
- can be serious / fatal
- stage 1 = tremors, sweating, agitation, increased autonomic reactions
- stage 2 = hallucinations and panic
- stage 3 = single / multiple grand mal seizures
lithium toxicity
- symptoms may mimic the flu
- vomiting, abdominal pain, severe diarrhea
- severe tremor, ataxia, coma, seizures, confusion, irregular heartbeat
Parkinson’s disease
- primarily considered a movement disorder, mask like expression in face.
- caused by loss of dopamine producing cells in the substantia nigra which affects functioning of basal ganglia
- characterized by tremors, rigidity, bradykinesia (slowed initiation of movement), and shuffling gait
- symptoms result from decreased levels of dopamine
- also see a degeneration of norepinephrine neurons in locus ceruleus (responsible for non motor symptoms- depression, cog deficits and sleep issues)
- apoe gene (higher risk for Parkinson’s, Lewy bodies, vascular and Alzheimer’s)
- more glutamate in basal ganglia at fault for progression of motor symptoms
hemispacial neglect
- one-sided neglect
- most often results from damage to the right hemisphere
- results in a lack of awareness of objects on the left side
contralateral vs. ipsilateral
contralateral = opposite side
ipsilateral = same side
Bottom-up vs top down
Bottom: starts with sensory —> brain (data driven)
Top: brain —> interprets sensory info (concept driven)
Neuroleptic malignant syndrome
-rare life threatening/lethal.
- Physio symptoms (muscle rigidity, mutism, joint pain, altered consciousness) + altered mental state and autonomic dysfunction (high BP, tachycardia, sweating, fever)
-treatment: stop taking drug at first sign and put on supportive therapy (hydrate+ cool off)
- MEN under 40** MORE at risk
- occur in 1st Gen (typical/traditional) or 2nd Gen (atypical) antipsychotics
Myasthenia Gravis
Ach receptors destroyed at neuromuscular junctions
Low GABA disorders
Insomnia seizures and anxiety
High glutamate disorders
Seizures, strokes, huntingtons and Alzheimer’s
Tourette
High dopamine in caudate nucleus
Low serotonin disorders
Depression, high risk for suicide, bulimia, ocd migraines
High serotonin
Anorexia (high in brain causing obsessive thoughts & anxiety… food restriction lowers serotonin/symptoms).
ASD & chronic schizo (higher levels in blood)
Homologous, compensatory, map expansion & cross modal
Homologous (same area opp side)
Cross modal (area now does something else since it was empty)
Map expansion (expands by recruiting from border)
Compensatory (compensates ability via other function like memorization when spatial abilities are impaired
Dopaminergic oathways (Mesolimbic, mesocortical, tuberofundibular, nigrostriatal)
Mesolimbic- reward pathway (VTA- ventral striatum)
Mesocortical- exec function, motivation and emotional reg (VTA-PFC)
tubero- hormone regulation (prolactin) (hypothalamus- pit gland)
Nigrostriatal- purposeful movement (substantia nigra-dorsal striatum (caudate nucleus and putamen)
Hemiparesis vs hemiplegia vs hemianopsia
Hemiplegia: paralysis
Hemiparesis: weakness
Hemianopsia: visual field loss
Middle artery vs posterior artery vs anterior artery symptoms post stroke (key distinctions)
All have contra lateral sensory loss, Hemiparesis (weakness)
Middle: aphasia (when dominant is affected), apraxia, contralateral neglect and weakness**. Most common.
Posterior: náusea/vomiting, memory loss, Anosognosia (denial about illness)
Anterior: impaired insight, amnesia, depression, judgement, mutism, apathy, confusion and urinary incontinence
PTE (post traumatic epilepsy) vs PTS (post traumatic seizures)
Pts (post traumatic seizures): seizures occur within 1 week of TBI. Treated well with anti seizure meds.
PTE (post traumatic epilepsy): seizures occur for + one week after TBI. Harder to treat, vagus nerve stimulation, responsive neurostimulation, surgery when meds don’t work.
Seizures (brain areas)
Temp lobe, hippocampal atrophy and in simple partial we also see frontal lobe involved in Jacksonian seizures.
Prognosis of TBI
anterograde amnesia duration
Most recover within 3 months & additional recovery within rest of 1st yr. Tho some may have injuries forever
Diabetes mellitus (type 1 & 2) vs central diabetes insipidus vs hypoglycaemia
Mellitus: not enough insulin, increases blood sugar levels. can be trigg by 2nd Gen antipsychotic (atypical) use. Type 1: autoimmune d cause destruction of insulin producing cells in pancreas (trigg by viral infection) type 2: pancreas doesn’t produce enough insulin
Central diabetes insipidus: ADH (pit gland)
Hypoglycaemia: too much insulin, low blood sugar
Neuroimages
NEBA: higher theta & beta wave ratio. Assist with ADHD diagnosis.
CT vs. MRI: mri preferred bc images are sharper/3D. Pros of CT: cheap, widely available. Cons: x-ray, MRI pro: better images con: have to stay still for long time
DTI: helpful to conj with ID of neurocog disorders, ASD, schizo, epilepsy & MS
FDG-PET: used to ID difference between Alzheimer’s and frontotemporal neurocognitive disorder
Side effects of 2nd Gen antipsychotics (atypical)
Neuroleptic malignant syndrome, metabolic syndrome (weight gain, high BP, insulin resistance, hyperglycaemia, increased risk for diabetes mellitus and heart disease), anticholinergic effects and agranulocytosis
SSRI side effects
Have a delayed onset (2-4 weeks sometimes 6-8 weeks for full effects). Also have suicidal ideation risk (especially for those under 24)
Mild anticholinergic effects, gastric problems, insomnia, anxiety, sexual dysfunction, weight gain.
Abrupt cessation: discontinuation syndrome (headaches, dizziness, mood lability, impaired concentration, sleep issues and flu like symptoms)
Can’t be combined with an serotinergic drug (MAOI, SNRI,TCA) : serotonin syndrome - potentially fatal (extreme agitation, confusion, autonomic instability, hyperthermia, tremor, seizures, and delirium.) Treatment: STOP
tachyphylaxis** (AD poop out, tolerance). Signs of this included: apathy, fatigue, imp. Cog functioning, sleep disturbance, sexual dysfunction. Treatment: increase dose, switch to different SSRi, SNRI (venlafaxine), TCA (clomipramine) which have lower rates of tachyphylaxis. Or combine with another med (TCA, bupropion, lithium, atypical antipsychotic) or depression focused therapy.
Tip: think of 7 SSSSSSS’s: sleep difficulty, size increase, stomach problems, serotonin syndrome, suicidal ideation (for under 24), stress/anxiety and sexual dysfunction
SSRI vs SNRI
Similar in efficacy. SNRI may be more effective for severe depression
SNRI side effects
norepinephrine: heart problems
Serotonin: same as SSRI discontinuation syndrome and serotonin syndrome
PTSD brain & neurotransmitters
High glutamate, norepinephrine and dopamine. Low serotonin and GABA
brain: hyperactive amygdala/anterior cingulate, hypoactive vmPFC, reduced volume of hippocampus. Research finds that in PTSD reduced activity in vmPFCreduces inhibitory top/down control of amygdala> exaggerated fear responses.
Cognitive appraisal theory (stress; primary, secondary and reappraisal)
Primary: what’s happening? Evaluate significance of situation. (Stressful/non stressful)
Secondary: what can I do about it? Stage involves assessing our ability to cope with/control situation. (Det what resources personal/environmental will be used)
Reappraisals: is my response appropriate? Ongoing. Make adjustments if necessary
Research on treatment effects of chemo and cranial irradiation in children’s neurocognitive functioning?
Both associated with deficits in neurocognitive functioning
Depression (heredity, neurotransmitters, brain)
Heredity: genetic link (higher rates in ID twins), larger rates for female pairs.
Neurotransmitters: low serotonin dopamine and norepinephrine
Brain: HPA axis (persistent hyperactivity/hypersecretion of cortisol associated with increased risk of depression). Abnormal activity levels in vmPFC & dlPFC.
Models for understanding depression (social reinforcement theory, learned helplessness model, Beck’s CT)
lewinsohn’s Social reinforcement: d. Results from low rate of response contingent reinforcement for social behaviours. Lack of reinforcement» social isolation, low self esteem and pessimism
Seligman Learned Helplessness: d linked to repeated exposure to uncontrollable negative life events. Reformulared version emphasizes: negative cognitive style= stable, internal and global. Hopelessness theory: describes hopelessness as cause.
Beck: depresion due to cognitive triad.
Sleep abnormalities in depression:
Reduced REM latency, prolonged sleep latency, INCREASED REM density, reduced slow wave sleep (stages 3/4),
Anxiety (brain, neuroimaging)
Brain: abnormalities in vmPFC, dlPFC, anterior cingulate cortex, posterior parietal cortex, amygdala and hippocampus.
Neuroimaging: Reduced connectivity bw PFC, anterior cingulate cortex and amygdala
OCD (brain)
Lower than normal levels of serotonin, elevated activity in caudate nucleus, orbito frontal cortex, cingulate gyrus and thalamus
Highest concordance rate is to what disorder
Bipolar
PFC damage (dorsolateral, orbitofrontal and Ventromedial PFC)
dorsolateral: role in executive functions, damage can cause concrete thinking, impaired judgment and insight, poor planning ability, deficits in working memory, perseverative responses*, and disinterest and apathy.
- causes dysexecutive syndrome. Decreased activity= depression. Think as exec part of brain.
Orbitofrontal: role in emotion regulation, response inhibition, and social behaviors. Damage can cause poor impulse control, social inappropriateness (e.g., immature behavior, offensive jokes), lack of concern for others, aggressive* and antisocial behaviors, distractibility, and affective lability*.
Ventromedial: role in decision-making, social cognition. Damage - impaired decision-making and moral judgment, lack of insight, deficits in social cognition (e.g., impaired emotion recognition, reduced empathy), confabulation, and blunted emotional responses.
- decreased activity= PTSD
Atypical parkinsonism
*contraindicated for DBS
involves symptoms that are similar to Parkinson’s but is caused by other disorders (Lewy bodies, progressive supra nuclear palsy, multiple system atrophy). But unlike Parkinson’s it DOESNT respond to treatment with dopamine (levadopa) or DBS***
What is an early sign of Alzheimer’s and what is a risk factor (hint: think of senses)
Sign: loss of smell
Risk factor: untreated hearing loss
Ataxia vs apraxia
Ataxia: think x for shouldn’t drink bc then you walk with ataxia.
- Lack of coordination in voluntary muscle movements.
- Affects balance, coordination, and can result in unsteady movements.
- Caused by damage to the cerebellum in the brain.
Apraxia: think p for purposeful movement
- Inability to perform purposeful movements despite physical ability.
- Disconnect between intention and execution.
- Can affect speech (apraxia of speech) or limb movements.
In response to a stressful situation the hypothalamus and the sympathetic NS stimulate which area of the brain to release epinephrine and norepinephrine?
Adrenal medulla
Recovery of cognitive functions following TBI (think PT)
Retrograde (oldest memories return 1st)
Orientation to personal information 1st, place 2nd then time as 3rd. Patients who continue to be disoriented to personal information rarely exhibit orientation to time/place.
Echolalia vs coprolalia vs echokinesis
Echolalia: repeat others vocalizations
Coprolalia: repeat socially undesirable words
Echokinesis: mimic others movements
Anosognosia vs prosopagnosia vs asomatognosia
Anosognosia: fail to recognize own illness/neurological symptoms (ie. paralysis)
Prosopagnosia: inability to recognize familiar faces
Asomatopsia: damage to somatosensory cortex. Unable to recognize parts of their own body.
Cingulate cortex (“cingle file”)
Think of the cingulate cortex as the emotional traffic controller in your brain. It helps regulate emotions, manage decision-making, pain, motivation and navigate the complexities of social interactions.
disruptions in the cingulate cortex can be linked to conditions like anxiety, depression, bipolar disorder and obsessive-compulsive disorder.
Damage: experience pain but not distressed by it
Supplementary motor cortex vs premotor cortex vs primary motor cortex in movements
Supplementary: planning & organizing movements (determine trajectory and bilateral coordination)
Premotor: prep and generate motor commands (receives sensory info and transforms to motor commands- bottom up)
Primary: executing movements (what it receives from premotor)
Research on stress and hippocampus size
Increased stress = increased cortisol impairs retrieval of declarative memories
Also it’s been found that in individuals with more trauma and ptsd= hippocampus size is smaller in volume. Therefore predisposing you to PTSD. Others say increased stress decreases volume and that leads to distressing memories from PTSD
Basal ganglia includes what 3 structures
Nucleus accumbens, putamen and caudate nucleus (all part of striatum and all receive input from cortex)
Globus pallidus: transmits info to thalamus (messenger of sense signals throughout brain)
Thalamus
messenger of sense signals throughout brain. All laterized except smell (ipsilateral). Also helps in sensory/motor functioning, language speech and declarative memory.
Damage: schizophrenia, confabulation syndrome (Korsakoff)= confabulation, thiamine deficiency, anterograde amnesia, retrograde amnesia
Split brain pick up/say things study cheat sheet
You see something in your left you won’t be able to SAY it but will be able to pick it up (bc Broca’s is laterized in 95% to the left for right handlers and 50% for left handers)
You see something to your right you will be able to SAY IT!
What 2 neurotransmitters are both inhibitory and excitatory
Dopamine and acetylcholine
Partial Seizures (simple partial/focal onset AWARENESS* seizures vs complex partial seizures/focal onset IMPAIRED AWARENESS* seizures)
Simple: DONT lose consciousness (only seizure type that doesn’t) and can describe seizures after. Jacksonian seizures are an example of this type of seizure and can happen in frontal lobe.
Complex: always lose consciousness, auras right before are common and automatisms (involuntary movements like pacing, fidgeting or walking in circles). Example: temporal lobe epilepsy
Alogia (negative symptom of schizophrenia)
Can speak but choose not to
Positive and negative symptoms of schizophrenia & BRAIN
positive symptoms via MESOLIMBIC pathway
Negative symptom via MESOcortical pathway
Serotonin syndrome (CAN)
Side effect of ADs. Think of CAN
- Cognitive changes: agitation, confusion, euphoria, insomnia, hypomania and hallucinations
- autonomic changes: sweating fever and tachycardia
- neuromuscular changes: seizures, tremors, difficulty coordinating movements
Serotonin discontinuation syndrome (FINISH)
Think FINISH.* Get this when you stop serotonergic drug abruptly.
F= flu like symptoms
I= insomnia
N= nausea/upset stomach
I = imbalance (dizziness)
S= sensory disturbances (tingling, numbness
H= hyperarousal (increased energy and anxiety)
In SNRIs you also have: hypertension, anticholinergic and tachycardia
MAOIs & side effects
MAOI: increase norepinephrine, dopamine and serotonin
Side effects: anticholinergic, hypertensive crisis, avoid tyramine foods, not good for OAs at falling risk, more likely to being on mania, weight gain, headaches, edema(swelling), paresthesia (pins/needles tingling), myoclonus (muscle spasm), insomnia, sedation, hypotension, serotonin syndrome. Not good for suicidal ideation.
TCAs & side effects
TCA: increases/blocks reuptake of norepinephrine, dopamine and serotonin
Side effects: anticholinergic side effects, hypotension, weight gain, memory issues, drowsiness, cardiotoxic, not good for those with heart conditions/high BP/suicidal ideation, sexual dysfunction, can lead to death if overdose.
Benzo side effects
Blocks reuptake of GABA.
Side effects: anticholinergic, drowsiness, weakness, confusion, agitation, memory problems, concentration difficulty, sexual dysfunction, rebound anxiety (if discontinued too abruptly, known as paradoxical reaction), easy to overdose, use with caution with OA bf they have higher risk of fractures, Cary accidents and cognitive impairments. Avoid with addicts due to addictive qualities.
- caution: mixing with alcohol = synergic effect (BAD, sum 2 parts greater). Can’t withdraw too quickly. Withdrawal can be FATAL.
Beta blocker side effects
Hypotension, bradycardia (slow heart rate), don’t give to people with asthma, insomnia, sexual dysfunction, nausea, dizziness, depression and memory impairment.
Work as antagonist for norepinephrine and epinephrine
Psychostimulant and non stimulant side effects
Both good for ADHD and narcolepsy
Side effects: risk of abuse/dependence, hypertension*, lowers seizure threshold, can make tics worse, if dose too high=tremors, paranoia irritability, if overdose= heart failure stroke and seizure, don’t prescribe for those with history of heart problems schizophrenia BP 1, may increase anxiety, decrease appetite
Mood stabilizer/anticonvulsants & side effects
Good for: BP, seizures, migraines, Major depressive disorder (lithium can help when ADs don’t respond), intermittent explosive disorder (lithium/carbamazepine)
Side effects: hypothyroidism, lithium toxicity (can be fatal, why you need to frequently monitor), polydipsia (super thirsty), polyuria (excessive urinating), weight gain, tremors, difficulty concentrating and memory impairment
- with lithium: need to avoid salt intake caffeine alcohol NSAIDs like ibuprofen/Tylenol. Also have metallic taste.
Migraine headaches with aura vs migraine headaches without aura
With aura: classic
Without aura: common
Ideopathic vs nocebo vs latragenic
Ideopathic= unknown origin
Nocebo= opposite of placebo, when you take a sugar pill and believe it will make you worse (vs good in placebo)
Latragenic= infections/complications caused by receiving medical treatment
Kandel research with sea slugs (aplysia)
Found that short term memory increased serotonin and long term memory created new synapses and changed structure of existing neurons
Temporal lobe personality
Paranoid, aggressive and argumentative
Most common type of synesthesia
Grapheme-colour synesthesia (see numbers as colours)
