Neuroscience 2

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Rooting reflex: diappears by 6 months (can be longer in breast feeding infants)
Moro reflex: Gone by 4-5 months
Absent or incomlete Moro is seen with UMN lesions
Asymmetric Moro --> braxial plexus palsy on side of poorly abducted arm
Palmar grasp reflex: Hand - gone by 6 months
Foot - gone by 12 months
Galant reflex: Gone by 3-6 months
3 month old infant: Social behavior
Vestibulo-ocular reflex evokes full range - eyes remain straight as head is moved side to side
Infant pulled to upright position - head will lag
Asymmetric tonic neck reflex: When head is turned - arm and leg on same side will straighten
Gone by 4-5 months
Do not disappear, but are overcome by voluntary control
Prevents child from rolling over
6 month old infant: Social behavior
Meaningful sounds
May be able to sit up w/o assistance
Lost Moro and ATN reflexes
Develops instinct to break a fall
Parachute reflex: Will extend arms if possibility of falling
Gone by 2-4 months
Reappears at 5-6 months
Landau reflex: When placed on stomach, child will raise head and arch the back
Begins at 4-6 months
Inhibited or suppressed by 3-3.5 years
12 month exam: Shyness - actually expected cognitive state
Many are walking
Parachute reflex
Pincer grasp
Propping reflex: When held under arms, baby appears to take steps
Disappears by 2-3 months
Reappears when baby ready to walk around 10 months
Apgar scale: Normal 7-10 (2 x 5)
HR, RR, muscle tone, color, reflexes
Assessed within 1 minute and at 3-5 minutes
Touch, smell, and taste are close to fully developed
5-6 weeks: Development - gross to fine; head to foot
Should be able to raise head and shoulders when face down
Hands usually in a fist
Able to visually track an object past midline
3-5 months: Able to hold head at 90 degree angle to floor
Exploratory behavior
Able to bear some weight
Hands not fisted
Can reach for and transfer objects hand to hand
Will make direct eye contact
Vocalizes and smiles
7-8 months: Upper body strength
Able to sit and may be able to get there on own
Fascination with objects - shapes, colors, textures
Attention span is increasing
9-10 months: No trouble getting into sitting position
Can hang onto a low table
Rudimentary problem solving skills
Three finger pincer grasp
Stranger anxiety
Separation anxiety
1 year: Walking
Two finger pincer grasp
Increase in tantrum behavior
2 years: Toilet training - 15-36 months
Beginning of symbolic thinking - books, words, pictures
Fine motor - able to draw a circle, build a tower of blocks (6)
Two word sentences
3 years: Able to draw a triangle
Ride a tricycle
Three word sentences
Threats to development: Genetic > Birth trauma > Metabolic, Infectious, Tumors, Teratigens (affect at 3-6 weeks gestation)
Trauma leads to increased motor difficulty compared to other causes of MR
Most common causes of infant head trauma: MVC, falls, abuse
Greater acceleration and deceleration due to head size
Deprivation: Opportunity for attachment is critical
Anaclytic depression: withdrawn, failure to eat, often mute
Failure to thrive: lack of growth, listlessness, delayed cognitive development
This baby eats
Caretaker neglect is most common cause
Classical conditioning: Pavlov
US, UR, CS, CR
Generalization
Aplysia
Transference, counter-transference
Extinction (habituation): decreased response process due to repeated stimulus without paired stimulus
Spontaneous recovery: After brief rest period, the CS will again elicit the CR but with less intensity for a shorter period of time
Discrimination: If similar stiumulus is paired with UCS, organism will only respond to CS
Sensitization: Response of an organism to an aversive stimulus
Causes habituation to occur over a much slower time period
Operant conditioning: the probability of a behavior reoccuring is directly related to the response it elicits from the environment
Procedural learning - utilizing implicit memory
Positive reinforcement: increase the probability of a behavior reoccurring
Negative reinforcement: Removal of an unpleasant stimulus in order to increase the probability that a behavior will re-occur
Positive punishment: response which decreases the probability of a behavior reoccurring
Negative punishment: Removal of a reward in order to increase the likelihood of the behavior occurring
Aversive punishment: Painful or noxious stimuli are used to deal with unwanted behavior
Fixed ratio: Behavior will increase in frequency rapidly
Behavior is extinguished rapidly as well when reward is removed
Continuous ratio - 1:1
Variable ratio: Most naturally occurring reinforcement schedule
Behavior is harder to extinguish
Shaping: successive approximations of the desired behavior following a hierarchy
Systematic reinforcement
Critical when behavior does not occur naturally
Procedural learning: Learning new behavioral responses as a result of reinforcement without necessarily being conscious or aware of the behaviors in question
Does not require verbal memory
Generalization: Behavior learned in one environment is applied in a different environmental context
Behavior more likely to be expressed within the environment within which it is learned
Modeling: Learned responses based upon the observations of others adapting to the same situation
Children and parents
Brain reward system: MFB, NA, VTA
Dopaminergic system
Addictions affect reward system - system responsible for creating addictive behavior
Involves the PFC
Earlier an addiction occurs the harder it is to deal with later
Systematic desensitization: Teach relaxation
Coincide relaxation with stimulus
Work on a hierarchy of stimuli
Abstract thinking: <25% of adolescents have capability of abstract thinking by 14
Adolescence: Tremendous growth in PFC
Emotional intelligence
Emotional intelligence: Perception - ventromedial
Assimilation - dorsolateral
Understanding - ACC, HC
Regulation - OFC
Developmental milestones: 2-3 - tolilet training, gender identity, parallel play
4 - cooperative play
6-11 - moral conscience (superego), identifies with same sex parent
Differentiation: Language - 6
Speech - 12
Working memory - 22
Developmental red flags: No real social behavior at 6 months

No sharing of sounds at 6 months

No babbling at 12 months

No gestures by 12 months

No words by 16 months

Any loss of speech at any age
IQ - Intelligence quotient: Mental age/Chronological age
Verbal IQ - LT hemisphere
Performance IQ - spatial/ visual
IQ mean = 100
<70 = MR
>130 = gifted
Cultural bias
Predicts educational achievement, but not vocational achievement
Does not assess creativity
Mini mental status: Orientation
Registration
Attention and calculation
Recall
Language - naming, repitition, 3 stage command, reading, writing, copying

Total score = 30
<23 = high likelihood of dementia
25-29 = normal aging or borderline dementia
Frontal assessment battery (FAB): Any score below 17 may indicate frontal lobe damage
TAN HATS: Thirts and water balance
Anterior pituitary control
Neurohypophysis (PP) control

Hunger and satiety
ANS regulation
Temperature regulation
Sexual urges and emotions
HAH: Olfactory cortex

Hypothalamus - visceral
Amygdala - emotion
Hippocampus - memory
Borders of hypothalamus: MOTT

Midbrain
Optic chiasm
Third ventricle
Thalamus
Endocrine hypothalamic nuclei: PAPPS
Supraoptic - ADH
Paraventricular - oxytocin
Paraventricular + REST - AP
Side effect of D2 blockers: Uninhibited release of prolactin
Control of appetite: Ventromedial - inhibits
Lateral - stimulates
Genetic disorders
- PW - paternal 15
- AS - maternal 15
Limbic system components: Cingulate gyrus
Parahippocampal gyrus
Amygdala
Hippocampus
Septal nuclei
Hypothalamus
Olfactory areas
Papaez circuit: Hippocampus - fornix - MB - anterior nucleus of thalamus - cingulate gyrus - entorhinal cortex - hippocampus
Role of hippocampus: Conversion of short term to long term memory
Conditions affecting hippocampus: Anterior choroidal infarct
Temporal lobe seizures
Toxins
Glasgow coma scale: Best eye response
Best verbal response
Best motor response

3-8 severe brain injury
9-12 moderate brain injury
13-14 mild brain injury
Severity judged by length of coma - >3 months - death
Ranch Los Amigos scale: Stages of coma recovery
Emergence from coma is accompanied by growing agitation
Predictors of outcome: Length of coma - motor recovery
Anterograde amnesia - cognitive
Structures most vulnerable to TBI: PFC - especially OFC
Temporal lobes
Limbic system/hippocampus
Hypothalamus
Long axons
Key diagnostic component and indicator of MTBI: AMS
Anterograde amnesia
PTA>30 minutes = TBI ~MTBI
Common anatomic sites causing contre-coup type lesions: Orbital plates
Crista galli
Sphenoid wings
Petrous ridges
Edges of falx cerebri
Edges of tentorium
- can injure corpus
callosum or cerebral
peduncles
Indicator of diffuse axonal injury: Amyloid precursor protein
Possible results of closed head injury: CHEF

Contusion
Hematoma
Edema
Fracture
MS: Loss of myelin and oligos
Perivascular lymphocytes
Oligoclonal IgG in CSF
Therpy using INF-beta
Natalizumab - inhibits migration of inflammatory cells
Cognitive dysfunction - IP, EF, V/S function
Detecting of axonal injury: MR spectroscopy using N-acteyl aspartate
Supply of thalamus/diencephalon: PCA, posterior communicating artery, (ACA)
Supply to deep nuclei of cerebellum: Superior cerebellar artery
Overlapping supply of the midbrain: Paramedian branches of PCA/Basilar

Long circumferentials/SCA
Origins of segmental arteries to spinal circulation: Intercostal
Lumbar
Sacral
Venous drainage of brain: Superficial/deep cerebral veins --> venous sinuses --> IJV
Acute lead poisoning: Marked brain edema, seizures, coma, death due to herniation
Chronic lead poisoning: HA, malaise, anorexia, abdominal pain, peripheral neuropathy

Children - neurobehavioral disorders and MR
Mercury poisoning: Personality changes, tremors, ataxia, visual loss

Destruction of granule cells in cerebellum, and of neurons in calcarine cortex
Arsenic poisoning: HA, drowsiness, confusion, delirium, seizures, peripheral neuropathy

Widespread petechial hemorrhages in white matter
Manganese poisoning: Interferes with AChEase and adenosine deaminase
Stimulates MAO
Extrapyramidal syndromes resembling Parkinsonism
Phosphorus and OP compound poisoning: Inhibitors of AChEase
HA, vomiting, sweating, abdominal cramps, miosis, and bronchospasm
Most symptoms can be reversed by atropine
Symmetric peripheral neuropathy - "dying back"
Wernicke's encephalopathy: B1 deficiency
Triad - confusion, ocular palsies, ataxia
Small hemorrhages in MB
Resembles SANE - affects young children, does not affect MB
Associated with Korsakoff's psychosis - irreversible
Central pontine myelinolysis: Due to rapid correction of hyponatremia
Acute pontine swelling -"grid" pattern of fibers makes them succeptible to compression
Quadriplegia of sudden onset with decreased consciousness
Alcoholic cerebellar degeneration: Loss of neurons in anterior vermis - loss of Purkinje and granular neurons
Truncal ataxia and wide based gait
Marchiafava-Bignami disease: Degeneration of corpus callosum and other commissural systems
M>>F
Epilepsy, ataxia, dysarthria, LOC, primitive reflexes
3 diseases producing Alzheimer type II cells: Hepatic encephalopathy
Wilson's disease
Severe chronic uremia
Hepatic encephalopathy: AMS and asterixis
Glutamic DH is increased
Wilson's disease: Defect in ceruloplasmin
Deposits in liver, putamen, and globus pallidus
Brain lesions are cavitary and brown
Rest tremor, slowness of movement, dysarthria, hoarseness, intellectual impairment, emotional lability
Kayser-Fleischer rings
Vessels more likely to sustain primary thrombus: ICA
VA
BA
Vessels more likely to have an embolus: MCA
ACA
PCA
Intracerebral hematoma: Most frequent underlying cause is systemic HTN
Saccular (berry aneurysms): Due to congenital attenuation of absence of media
Association with polycystic kidney disease
Duret hemorrhage: secondary to increased ICP and herniation
Direct cause of death in patients with supratentorial mass lesions or swellings
Charcot-Brouchard aneurysms: Swellings of small perforating arteries
BG/thalamus > pons > cerebellum > cerebrum
Most common - LS arteries; also most common site of lacunar infarct
Proportion of sleep: 75% NREM
25% REM
Polysomnogram: EEG
EOG
EMG
REM: EEG desynchronized
EMG atonic
HR irregular
RR irregular
BP variable
CBF and metabolism increased
Poikilothermic
Positive tumescence
NREM: EEG synchronized
EMG tone present
HR regular
RR regular
BP regular
CBF and metabolism reduced
Homeothermic
Negative tumescence
Circadian rhythm: SCN
Nap at temp max
Sleep at temp nadir
Afferent - retinohypothalamic
SCN --> sympathetic NS --> pineal --> melatonin
Efferent - to pineal gland
Factors affecting circadian rhythm: Light - duration and intensity
Food
Activity/exercise
Ambient temperature
Melatonin: Greatest release nocturnal
Light blocks release
Promotes sleep, affects brainstem, anti-gonadotropic
Multiple sleep latency test (MSLT): 4 or 5 nap opportunities after night of PSG
Latency to first epoch of sleep measured
>10 = normal
< 10 = sleepy
Cataplexy: REM atonia intruding into wakefulness
Occurs in emotional situations
Diagnosis of narcolepsy: Clinical + MSLT
May be CSF test in future - decreased HCRT in CSF
Shorted mean sleep latency <5
MSLT shows 2 or more SOREMPs
Restless legs syndrome: CARP FIPP

Chronic renal failure
Anemia
RA
Pregnancy

Folate deficiency
Iron deficiency
Peripheral neuropathy
Peripheral vascular disease
Psychophysiologic insomnia: Hyper-arousal state
Sleep state misperception: Patients believe they are not sleeping
Normal in sleep lab
Sleep wake transition: Myoclonic jerks with onset of sleep - normal
May be accompanied by sensation of falling or flash
Sleep terror: NREM
ANS hyperactivity
No recall
First half of night
Nightmares: REM
Vivid recall and narrative
More often second half of night
REM sleep behavior disorder: Dream enacting behavior during sleep
Loss of normal REM atonia
M>W
>50 years old
DA related
Correlates with ND diseases
Non-linear aspects of brain development: Front to back
Frontal, parietal --> temporal --> occipital --> cerebellum
False positives on MMSE: Depression
Low education
Focal brain lesions
Closed head injury: More common
Diffuse damage
More deficits upon recovery
Open head injury: Prone to infection
Higher initial mortality
Focal cerebral damage
Good prognosis for adaptation to cognitive impairments
Diffuse axonal injury: Long axons most vulnerable - communicating axons
Deficits in higher order cognitive activities
Damage to orbitofrontal regions of frontal and temporal lobes: Deficits in emotional control and memory
Increased extracellular K+: Released from glial cells and neurons
Convulsions
Vascular constriction
MTBI: Not likely to see physical limitations
Affective response is more severe
Metabolic cascade of MTBI: Vascular constriction
Increased demand for glucose and O2
Neurotoxic metabolites
CP450 reduced and then increased
Risk factors for PCS: Prior concussion
Brain lesions
APOE4
Distinguish psychiatric depression from neurologic depression: PD - loss of appetite, agitation, loss of interest in life
Distinguish contusion from old infarct: Contusion - tips of gyri
Infarct - depths of sulci
Degenerative diseases - mechanisms of injury: Accumulation of toxic proteins - beta-amyloid, tau
Accelerated apoptosis
Generation of free radicals
Development of inflammation
Alzheimer's disease: 5-10 year survival
May spare occipital lobe
Hydrocephalus ex vacuo
Neuritic plaques with amyloid core
Neurofibrillary tangles in neuronal cytoplasm
Amyloid deposits in vessels
NFT - formation of hyperphosphorylated tau
Alpha secretase cleavage results in soluble form
Presenilins regulate apoptosis
Aging brain: Granules surrounded by vacuoles
Mainly in hippocampus
Purano bodies
Pick's disease: Severe atrophy of cerebrum
"Knife-blade"
Hydrocephalus ex vacuo
No senile plaques
Pick bodies - tau protein
Frontotemporal dementia (FTD): Disinhibition, depression, Parkinsonism
AD - 17 (tau mutations)
Frontotemporal atrophy
Neuron loss in SN and cortex
NFT in neurons
Cortical basal degeneration: Onset as movement disorder - rigidity, dystonia
Apraxia, cortical sensory loss, alien hand
Atrophy of motor and sensoy cortex - more sensory + SN
Ballooned neurons
Astrocytic plaques - tau
Diffuse Lewy Body Disease: Dementia > Parkinsonism
More rapid course than Parkinson's
Lewy bodies in cortex and SN
Lewy bodies contain alpha-synuclein
Multiple system atrophy: Dementia + 1 or more features
Striatonigral - no Lewy bodies, L-dopa resistant
Shy-Drager - ANS dysfunction - postural hypotension - intermediolateral column
Olivopontocerebellar atrophy
Inclusion occur in neurons and oligos - resemble AD
Criteria for depression: Fatigue
Feelings of worthlessness
Diminished ability to concentrate
Recurrent thoughts of death
Greatest loss of brain in age related brain size decrease: Frontal lobes
Parietal lobes
Hippocampus
Lewy body disease: Buzz word - visual hallucinations
Vascular dementia: Patients retain awareness of deficits
Prone to depression
Suspiciousness of others
Bowel and bladder control issues

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