275 Review and Neuropsychological Assessment Flashcards

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1
Q

dorsal visual stream

A
  • processes visual info about where something is in space to help plan motor coordination
  • runs up the back of the brain, from occipital to parietal lobe
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2
Q

ventral visual stream

A
  • processes what objects are, basic shape, recognition and identification
  • runs occipital to temporal, through the lower regions
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3
Q

somatic nervous system

A
  • involved in creation of action (efferent, multipolar motor neurons) and sensation (afferent, unipolar sensory neurons that transmit infor back into the brain)
  • the two above are spinal nerves, but SNS also includes the cranial nerves
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4
Q

autonomic NS

A
  • two branches, parasympathetic (rest and digest, cal, balanced state) and sympathetic (fight/flight, increased heart rate, blood flow and muscle oxygenation, breathing)
  • mostly controlled through the hypothalamus, which has a direct neural connection to the pituitary gland and endocrine system (for release of adrenaline, cortisol, etc)
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5
Q

brain protection

A
  • the skull
  • the meninges (the hard dura mater, the arachnoid membrane and subarachnoid space (webby, well irrigated with CSF) and the pia mater)
  • the CSF, a fluid that surround the brain and gives it some buoyancy
  • the BBB (prevents toxins, viruses, certain bacterial from entering the brain)
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6
Q

blood supply

A
  • 2 carotid and 2 vertebral arteries supply blood to the brain
  • they run up the neck and connect at the base of the brain before splitting off into 3 new pairs: anterior cerebral artery (irrigates medial and dorsal parts of cortex), meddle cerebral artery (irrigates lateral surface of cortex) and posterior cerebral artery (ventral and posterior surfaces of cortex)
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7
Q

ventricles

A
  • the CNS has 4 (left and right lateral ventricles, then 3rd and 4th), and is a free flowing system for distributing CSF
  • the epithelial cells in choroid plexuses manufacture and secrete CSF, and monitor the pressure in the system
  • the masa intermedia, which bridges the two lobes of the thalamus (relay station), runs through a hole in the 3rd ventricle
  • the dural sinuses are cavities linked via the subarachnoid space that drain excess CSF into the jugular veins to be removed through the blood system and recycled

hydrocephalus: if there’s a blockage in the system, the ventricles won’t stop producing CSF even if the system registers the pressure getting too high, causing them to balloon out and exert pressure on surrounding brain tissues; the longer this continues, the greater the risk of damage.
- if there’s a leak (for example from a spinal tap), CSF may be lost, leading to headache that’s worse when sitting up, nausea, vomiting, funny eye mvmts

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8
Q

medulla

A
  • responsible for rudimentary survival function (respiration, heart rate)
  • where motor fibres cross (contralateral info)
  • responsible for reaction formation
  • location of reticular activating system (RAS) which is a web of nuclei involved in arousal and other functions
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9
Q

pons

A
  • ventral component of the brainstem
  • bridge of communication from the motor system to the cerebellum and back
  • signals for maintenance of equilibrium, balance, feedback of action and adjustment route from the cerebellum through the pons and up into the brain
  • also play a role in basic perception of timing
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10
Q

midbrain

A
  • on the dorsal side of the brainstem, location of the superior colliculi (higher up, receives 10% of info directly from eyes and produces quick, orientating, reflective response to vis info) and inferior colliculi (ditto but for sounds)
  • the combo of these two structures is also called the tectum
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11
Q

thalamus

A
  • relay centre of the brain
  • 2 lobes (one per hemi)
  • all sensory info routes here before primary cortical regions (except olfaction, which goes to O1 first then the thalamus)
  • also relays communications throughout the brain (interlobe, etc)
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12
Q

reticular formation

A
  • involved in arousal (continuous stimulation will render an animal unable to sleep while severance will render them comatose)
  • also important in pain signaling (alerts brain that pain messages are coming, which makes it a good target for some anesthetics)
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13
Q

substantia nigra

A
  • produces DA, very important region wrt the PD process, as these regions degenerate and don’t recover
  • creates lots of DA that interacts with tracts to basal ganglia (motor action centre)
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14
Q

red nucleus

A

output and integration of motor action

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15
Q

periaqueductal grey

A

responds to endorphins via opiate receptors; can play a role in blocking pain signals (gate controlled theory of pain-blocking message from entering the brain for processing)

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16
Q

cerebellum

A
  • densely packed structure that contains approx 60% of the brain’s cells
  • contains 2 lobes and has a functional mapping of the body analogous to the motor/sensory strips (regions of activation are functionally particular to certain areas of the body)
  • plays a role in balance, equilibrium, feedback to higher motor areas to keep things on track
17
Q

forebrain structures

A

basal ganglia and limbic system (which make up the subcortical regions), and he cerebral cortex

18
Q

basal ganglia

A
  • collection of nuclei (putamen, globus pallidus, caudate) which receive input from all area of the brain to control and coordinate movement patterns
  • has no direct connections to higher/frontal regios (comms must be routed via the thalamus back to motor cortex for any sort of accommodations or changes)
  • also plays key component in implicit motor memory
  • huntington’s has a direct damaging effect
19
Q

limbic system

A
-plays role in motivation, emotional processing, fear, anger 
includes amygdala (emotion and species-typical behaviours), hippocampus (memory formation/consolidation to LT store, abil to learn/rehearse/work info, spatial memory and nav), septum (processing relaying info the cingulate cortex) and the cingulate cortex/gyrus (deep in frontal lobe, plays role in response inhibition, cognitive flexibility, emotion, executive function, motor control)
20
Q

cerebral cortex

A
  • neocortex, the most upper regions of the brain
  • expanded the most during evolution and comprises 80% of the human brain
  • not all that thick, but huge surface area due to convolutions
  • six layers
  • two cerebral hemispheres, four lobes
21
Q

fissures/sulci/gyri

A

fissure: cleft in cortex deep enough to indent ventricles
sucus: shallow cleft in cortex
gyrus: ridge in cortex

22
Q

layering in the neocortex

A
  • 6 different layers; thickness with vary with area in the brain
  • layer IV takes in afferent info, so it will be thicker in sensory regions and primary regions
  • layer V sends efferent signals, and is therefor thicker in motor areas which have a high lvl of output
  • relaying of info can also happen in VI
  • layers predominantly house cell bodies which have no myelination, making this grey matter (once axons exit the layers, we start to see myelination)
23
Q

brodmann areas

A

areas that brodmann sectioned off the brain based solely on the structural differences in the order of cortical layers
-these later mapped very well onto the areas deemed to be involved in particular functions

24
Q

brenda milner

A
  • canadian neuropsych who worked with patients like HM to assess what deficits arose in patients receiving neurosurgery and the impact of damage in brain structure
  • firm believer that the right hemisphere wasn’t just a spare tire
25
Q

case of HC

A
  • 5 y/o boy with severe seizures from the LH impairing function to the pt that they removed the whole hemi
  • the seizures minimized immediately and abated after 3 mo
  • loss of sight in RVF (bc the vis system is pretty hardwired by 5, and RV1 couldn’t be compensated for in LH, but no neglect (fully attentional ability))
  • only persistent motor impairment was slight limp in right leg (compensation)
  • went on to graduate uni and became a high functioning corp exec
26
Q

mass action approach

A

-belief that extent of damage is more important than locus, and that any region in the brain could be involved in any function, so if one portion was removed, the rest had full plasticity to recover from it

27
Q

localization of function approach

A
  • penfield would perform surgery on patients and look at the differences btw function before and after to draw conclusions abt location of removal and function
  • studies in non-human animals suggests there’s a functional mapping along the anterior intraparietal (AIP) sulcus to do with more complex actions
28
Q

modularity of mind approach

A
  • a compsci perspective
  • the idea that there may be certain encapsulated processes or networks that form in the brain, neural networks for essential, automatic, fast, and highly specialized systems
  • ex. v few things other than faces will activate the fusiform area
29
Q

causes of malfunction in the brain

A

-closed head injury (jostling of the brain as it accelerates and decelerates inside the skull)
-cerebral oedema (swelling in the brain that can put pressure on and damage tissue)
-infarctions (neuronal degeneration or necrosis due to loss of blood supply as result of thrombosis, ischaemia)
-thrombosis (clotting of blood that can block arteries, or emobolism, in which fatty plaque buildups travel into the brain)
-stroke (sudden loss of blood supply; can be ischaemic (blockage cuts off supply to tissues) or hemorrhagic (break in the artery))
-tumour (encapsulated (solid mass w/in the tissue) or invasive (growing into the surrounding area))
-anoxia (complete lack of O2 leading to necrosis)
-encephalopathy (inflammation caused by toxic or physical agents like CO)
-encephalitis (inflammatory immune response)
hydrocephalus (pressure buildup from too much fluid in the free-flowing ventricular system)
-surgery (any sort of neurosurgery creates a lesion)

30
Q

lesion method in patients with circumscribed brain damage

A

looking at the relationship between structural brain damage and function
two approaches:
-neural substrate method (knowing where the damage is, look at cognitive function and corresponding deficits) ((ex galen, who knew gladiators were getting head injuries in fights, looked to see what deficits this gave rise to))
-cognitive function (looking at the deficits and seeking related regions of brain damage (often the case for people who have no clear surgical outlines and are just presenting with cognitive deficits))

31
Q

clinical neuropsychological assessment

A
  • a cognitive capacity profile that determines deficits as well as areas that seem unaffected
  • looks at language function, mem, spatial ability, etc
  • provides a baseline which is useful for rehab assessment and give a timeline of progression)
  • gives an idea of prognosis (where can we go from here, and was can we expect?)
  • done in conjunction with a full neurological exam (imagine to find extent of damage, background info from the patient/PG/family (to get sense of premorbid functioning))
32
Q

MMSE (mini mental state exam)

A
  • quick, rudimentary assessment, often done by ER physicians for suspected head injuries or patients who were briefly unconscious
  • orientation (year, mo, day, season; where are we and what makes you think that?)
  • registration (name/point to 3 unrelated objects and have them repeat back, may also probe by asking if they understand the function but couldn’t repeat the word; presented later as a recall task)
  • attention and calculation (can you spell this backwards, can you count backwards by 7s)
  • language (naming, execution of 3 stage command, repetition of phrases, writing spontaneous sentences (if they can’t write, can they speak it?), copy geom figures))
33
Q

test batteries

A
  • a group of tests used together to give ideas of general function
  • may be standardized (to distinguish btw symptoms due to brain injury and those that aren’t by looking at comparative norms), individual (pull in tests designed to probe deeper and gain qualitative info for unique problems, don’t usually have comparative norms) or composite (incorporating both standardized and individualized/specific tests)
34
Q

halstead-reitan battery

A

-standardized battery consisting of 11 tests (including: abstract reasoning (categorization), factual performance (fit cutouts into holes w/o sight), rhythm test, speech perception, 10s finger tapping, trail making, MMPI, WAIS)

35
Q

rey complex figure

A

test used in neuropsych assessment; have them try to copy down a very complex geometrical image, score this, then distract them a while before asking them to draw it back from memory (score again based on number of features and time to completion)

36
Q

raven progressive matrices

A

3 x 3 patterns; looking at the info given, determine which item from a bank completes the sequence
-looks at computational and cognitive function, and identifies areas to delve deeper into

37
Q

types of validity

A

construct: does it test the targeted cognitive function? (necessary for any test)
localization: does it reflect focal lesions (show exact specificity of brain damage, ex broca’s area tests)
diagnostic: dose it diagnose disease? (often requires a battery of tests)
ecologic: does it predict everyday-relevant behaviour (does it tell us how well that person will do back in the real world)

38
Q

experimental psych vs neuropsych assesment

A
  • resilient volunteers vs sensitive patients
  • for research vs application
  • looking at many vs indv subjects
  • looking at aggregates of average behaviour vs specific disorder behaviour
  • using many stim/trials vs few
  • long vs short time per test
  • striving to avoid false positives vs false negatives
  • findings with small but statistically significant effects vs big effects that aren’t necessarily stat significant
  • testing hypothesis abt brain function vs dysfunction
39
Q

case of AL

A
  • AL slipped on the playground, fell on his back and suffered a concussion; he sued school board claiming cog issues (nausea, depression, mem and attention problems)
  • neuropsych assessment revealed mild impairments on broad range of tests, esp response time, but the only severe score was vis impairment
  • are the deficits premorbid, due to the injury, or the result of functioning? do we have all the info necessary to make valid conclusions?