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PSYCHOLOGY SEM 1 YR 1 > PYB102 > Flashcards

PYB102 Flashcards

1
Q

Tracts, nerves, nuceli, ganglia

A

Tracts: groups of axons in CNS

Nerves: groups of axons in PNS

Nuclei: groups of neurons in CNS

Ganglia: groups of neurons in PNS

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2
Q

Developing Neural Tube

A

Neural crest: forms the PNS

Neural tube: forms CNS

Top part of neural tube: forebrain
Middle part: midbrain
Bottom part: hindbrain
Developing spinal cord

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3
Q

Hindbrain Regions

A

Medulla: heartrate, blood pressure, respiration
- Pyramidal tracts on ventral surface of medulla
- Olivary nuclei lateral to pyramidal tracts (superior-sound localisation, inferior-unknown)

Axons travel from the cortex to pons to the medulla, crossing over in an act of decussation when they reach the medulla. This means that the tracts from the left side of the brain spread down the brainstem and control the right side of the body

Pons: Connects brainstem with cerebellum
- Consciousness and alertness

Cerebellum: co-ordination of balance and movement (left side of cerebellum controls movement on right side of body etc)

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4
Q

Midbrain regions

A

Superior colliculi: visual info

Inferior colliculi: auditory info

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5
Q

Forebrain (Diencephalon)

A

Hypothalamus: basic drives (fight, flight etc), control autonomic nervous system (sympathetic, parasympathetic nervous system), controls hormones/endocrine system by sending signals to pituitary gland which releases hormones

Thalamus: relay of sensory info the cortex (expect for smell, which is done by olfactory bulb)

Corpus callosum: white matter tracts

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6
Q

Forebrain (Telencephalon)

A

Limbic system (learning, memory, emotional expression)

Basal Ganglia: planning and producing movement

Amygdala: fear learning, emotional info

Hippocampus: memory and making new memories

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7
Q

Cerebral Cortex Lobes

A

Frontal lobe: movement, motor control, higher-order cognition, executive functions

Parietal lobe: Sensory info

Occipital lobe: visual info

Temporal Lobe: auditory info, memory functions

Longitudinal fissure: deep groove between two cerebral hemispheres

Lateral fissure: deep groove on the of the brain

Central sulcus: groove between parietal and frontal lobe

Primary Motor cortex: located anterior to the central sulcus
- corresponds to motor control in each part of the body

Primary somatosensory cortex: located posterior to the central sulcus
- sensory info attributed to each part of the body

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8
Q

Contralateral arrangement

A

Right visual field is projected to left occipital lobe etc.

Right visual info from both eyes goes to left occipital lobe via the corpus callosum

Split-brain experiments
- Severed corpus callosum to stop info from being transferred via corpus callosum to opposite lobe

  • Patients could only see the words/ info in right visual field (meaning that the left occipital lobe was more lateralised to processing visual info)
  • Therefore, left hemisphere is more lateralised to processing language whereas the right hemisphere more lateralised to motor control over the body (tested by getting subject to pick up item with left hand)
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9
Q

Cerebral Ventricles

A

Lateral ventricles
Third ventricle
Fourth ventricle
FILLED WITH CEREBROSPINAL FLUID (for exchange of nutrients, minerals, and is a shock absorber)

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10
Q

Meninges

A

Dura mater
Arachnoid membrane
Sub arachnoid membrane
Pia mater

Choroid plexus: creates cerebrospinal fluid

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11
Q

The vascular system

A

Blood-brain barrier protects the brain from flowing of toxins, but can inhibit drug flow into brain

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12
Q

Divisions of the CNS: Spinal cord

A

Afferent nerve/dorsal (arrive to spinal cord): carries in sensory info to the brain via spinal cord

Efferent nerve/ventral (exit the spinal cord): carries motor info away from brain into the body

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13
Q

PNS

A

Somatic nervous system

Autonomic nervous system: Sympathetic: spending bodies energy (dilates pupil, more heartbeat, relaxed breathing/more breathing, inhibits activity, contracts blood vessels)

Parasympathetic: contracts pupil, constricts breathing, slows heartbeat, stimulates activity, dilates vessels

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14
Q

Neurons

A

Reception: take in info from other neurons via the dendrites and soma

Conduction: action potential travels along axon

Transmission: pass it on to other neurons (who receive it with their terminal buttons)

Pre-synaptic neuron
Post-synaptic neuron

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15
Q

Glial cells

A

Nourish and protect neurons

Oligodendrocyte glial cells: create myelin sheaths around axons of neurons, to facilitate conduction of action potentials across the axons

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16
Q

The cell membrane

A

Lipid bilayer that has protein channels

Resting membrane potential: difference in chemical composition inside and outside of membrane
- approximately -70mV, but needs to be down to -55mV for an action potential

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17
Q

The neuron at rest

A

Protein channels are closed

Causes a resting membrane potential of -70mV

Creates a difference in electrical charge and concentration of ions on either side of the membrane

Na+ has greater concentration outside of cell

K+ has greater concentration inside of cell

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18
Q

Action potential

A

sufficiently de-polarized to -55mV

when reaching -55mV, an action potential will be generated by the reversal of the resting potential

action potential always the same size (all or nothing principle)

  1. sodium channels open
  2. potassium channels open
  3. sodium channels close
  4. potassium channels close
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19
Q

Speeding up action potentials

A

Myelin sheaths: action potential forced to jump between nodes and travel down axons faster as the myelin sheath is an insulator which does not carry electricity

Axon diameters: quicker action potentials

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20
Q

Process of synaptic transmissions

A

Action potential travels along axons and reaches terminal buttons

Terminal buttons release neurotransmitters into the synapse

They are received by the next neuron’s dendrites

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21
Q

Neurotransmitters

A

Excitatory: binds to post-synaptic cell receptors and causes it to depolarise

Inhibitory: binds to post-synaptic cell receptors and causes polarization

Binding of neurotransmitters to post-synaptic cell causes protein channels to open and influences the membrane potential

Removal of neurotransmitters:

Reuptake: taken back into pre-synaptic neuron

Enzyme degradation: enzyme breaks down the neurotransmitter and changes it so it cant be recognised

Diffusion: neurotransmitter released

Auto receptor: pre-synaptic neuron takes in the neurotransmitter and changes function of buttons so it wont be released again

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22
Q

The role of attention in encoding

A

Attention filter: stops overstimulation

is a filter of further processing of stimuli (stimuli is processed all the time but the filter only allows a certain amount of stimuli to get further processed)

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23
Q

Model of selective attention

A

Does attention to stimulus occur in the early selection (before we recognize the stimuli’s meaning)

or the late selection (after we recognise its meaning and filter out what’s important)?

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24
Q

Cocktail party phenomenon

A

Attention filter comes after recognition of meaning

Conclusion: there may be flexible selection, if filter can be before and after recognition of meaning, then attention filter may be flexible to suit different scenarios)

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25
Q

Enriching encoding + Craik and Tulving

A

Maintenance rehearsal: repetitive info, but doesn’t necessarily enrich encoding

Elaborative rehearsal: thinking about what you are trying to rehearse (enriches encoding)

Visual imagery: picturing/visualising info related to the things you are trying to learn

Self-referential encoding: applying info to yourself (associating with things you can relate to)

Craik and Tulving: Yellow words: superficial
Orange words: phonological qualities
Red words: semantic properties

We are more likely to remember semantic words (words with meaning provide richer encoding)

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26
Q

Memory storage - Sensory Register

A

Iconic memory: 9-10 items, 0.5 secs

Echoic memory: 5 items, 2 secs

Sperling’s whole report task: ask question: can people only remember 4.5 letters on average, or is this a matter of visual scanning limitations?

Sperling’s partial position report task: reducing memory workload meant that participants could recall 3 out of 4 letters in any row. This shows that memory is a limitation in this task. Therefore, we are seeing more items than we can recall

Sperling’s partial category report task: People didn’t recognise difference between numbers or letters. Shows that echoic memory doesn’t process meanings of symbols, rather it just processes raw visual image.
We need to go further in the process to recognise stimuli

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27
Q

Memory Storage: Short term memory

A

Traditional view: Duration of memory can exceed 20s through rehearsal
Without rehearsal: info decay
Info lost through: interference

Dual task technique
- digit span task and grammatical task
- tested how long it took to complete task while they tried to hold digits in their short term memory
- FINDINGS: short term memory can complete 2 tasks at once

Working memory model
- phonological buffer (auditory info manipulation)
- visuospatial sketchpad (setting up and manipulating visual images)
- central executive

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28
Q

Memory Storage: Long Term memory

A

holds info for days, weeks, months, years

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29
Q

Declarative memory

A

You can declare things you know facts, events)

Episodic memory: mental time travelling into past and future)

Semantic memory: generalised memory, knowledge, concepts, facts)

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30
Q

Non-declarative memory

A

Things you know that you show by doing

Skill learning

Priming: more likely to use a word you have heard recently

Conditioning: conditioned associations, conditioned behaviours

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31
Q

Anterograde amnesia

A

Loss of memory after event

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32
Q

Retrograde amnesia

A

Loss of memory before event

33
Q

H.M case study

A

Bilateral medial temporal lobectomy (removing portions of both temporal lobes, including hippocampus, amygdala, and rhinal cortex)

His STM and motor abilities preserved

He had retrograde and anterograde amnesia

Due to hippocampus being removed bilaterally, they believed that this caused anterograde amnesia (loss of ability to make new memories, hence hippocampus associated with memory making)

34
Q

Understanding H.M’s amnesia

A

Overall conclusion: non-declarative memory is stored differently to declarative memory, as H/M’s non-declarative memory was never disrupted

Digit span test: remembering a new set of digits every time to test STM (his STM was intact as his performance was good in these tests)

Digit span +1: remember same set of digits each time but +1. The +1 remains in STM, but the previous digits which are rehearsed over and over require LTM. His performance was bad due to bad LTM

Block tapping memory test: like digit span +1 but more visual. Ask people to tap blocks in order but +1 each time (he couldn’t create visual memories)

Mirror drawing test: easier with practise, drawing a picture using a mirror reflection. H.M became advanced at this task over time (intact non-declarative memory), despite him not recalling having done it the previous day (flaw in declarative memory). THEREFORE he has anterograde amnesia for declarative, not non-declarative memory

Incomplete pictures test: showing unfinished pictures and asking someone to complete or interpret them. He couldn’t remember doing this task previously

Floor plan…. was also accurate to his house. He couldn’t remember any explicit details, like address, number etc. But his spatial location and visual memory (non-declarative) allowed him to implicitly remember his house layout.

35
Q

Testing amnesia using monkeys: Delayed non-matching to sample task

A

Removing different parts of the monkey’s brain

Monkey presented with food under key initially and is trained to see association between key and food.

Delay presented so that LTM is tested, not STM: new object is also presented

Non-declarative memory: shown if monkey continues to move key to find food. Shows a conditioned association between food and key, and a learned skill/aka non-declarative memory

Declarative memory: shown if the monkey learns a new association between food and new object by moving new object instead of key

Results of brain damage:
Perirhinal cortex: severe damage
Bilateral Hippocampus: moderate damage
Bilateral amygdala: no damage

MAIN CONCLUSION: damaging hippocampus is not only source of amnesia

Damaging Perirhinal cortex disrupted sending of info to hippocampus, destroying any new info in hippocampus, and therefore disrupting formation of new memories

35
Q

Hippocampus function

A

Receiving info from Perirhinal cortex and forming new memories off it

Memory retrieval by retrieving memory out of cortex

Spatial info storage

36
Q

Sleep Stages

A

Alert wakefulness: beta waves

Just before sleep: alpha waves

Stage 1: theta

Stage 2: theta + k complex high amplitude + low frequency waves every now and then + sleep spindle (rapid bursts of EEG activity)
Physiological experience: hypnic jerk (your body wakes you up before you fall asleep, potentially from your reticular formation regulating your level of arousal, the transition from asleep to awake, brain may mis-interpret sleeping as dieing and therefore tries to reboot your body back to life, hence the hypnic jerk

Stage 3: delta
SWS (slow wave sleep) - difficult to wake someone up in SWS, if you wake up during SWS you will feel so unwell (big transition from SWS to awake stage can exhaust you)

Stage 4: delta

REM sleep: theta and beta
Lack of any muscle activity in REM sleep, you are almost paralysed
EEG in REM sleep similar to EEG while awake

37
Q

EEG, EOG, EMG

A

Electroencephalography

Electrooculogram (eye movements)

Electromyogram (muscles under chin)

38
Q

Sleep patterns through night

A

Visit multiple periods of stage, 1, 2, 3, 4 sleep which transition into REM sleep throughout the night. These stages are visited in various orders throughout the night

39
Q

Age dependent sleep

A

As we are older we need fewer hrs of sleep plus get less REM sleep

40
Q

NREM vs REM sleep physiology

A

Brain activity: decreasing from wakefulness (NREM), increasing motor and sensory areas (REM)

Heart rate: decreasing from wakefulness (NREM), increasing (REM)

Blood pressure: decreasing from wakefulness (NREM), increasing (REM)

Blood flow to brain: decreasing from wakefulness but not in most regions (NREM), increasing in certain brain regions (REM)

Respiration: decreases (NREM), increases (REM)

Body temp: is regulated (NREM), is not regulated/no shivering or sweating etc (REM)

41
Q

Sleep in animals

A

Unihemispheric

42
Q

Brain regions important for circadian rhythm and REM sleep

A

Suprachiasmatic nucleus: structure in hypothalamus which entrains (resets) our circadian rhythm. Light falling on our retina sends signal to suprachiasmatic nucleus which resets our rhythm

Retinohypothalamic pathway: optic nerves (PNS) run from eye retinas to optic chiasm

optic tracts (CNS) run from optic chiasm to suprachiasmatic nucleus

43
Q

Damage to brain regions that regulate sleep

A

Damage to optic nerve or retinas: light signals will not reach the suprachiasmatic nucleus because that pathway had been damaged, causes our circadian rhythm to be FREE RUNNING and not entrained

Damage to optic tract or occipital lobe: entrainment will occur because light signal pathway through optic nerve to suprachiasmatic nucleus is not destroyed. However, this will cause visual impairment because visual signals will not be processed by cortex or wont be sent to cortex via tracts

44
Q

Pons in sleep

A

Pons: consciousness and alertness

Trigger REM sleep by sending upward signal to cortex (triggers dreaming) and sending downwards signal to body (muscle paralysis)

REM sleep behaviour disorder: people actually acting out their dreams (the descending signal to cause muscle paralysis becomes atypical)

45
Q

Amnesia in sleep

A

Selective sleep amnesia: from period of wakefulness to sleep

Our brain causes us to forget our dreams when going from sleep to wakefulness to prevent us from mixing up our real world reality with what happened in our dreams

If waking up during REM sleep stage, we can instantly report our dream, however, if you wake up during the night and go to sleep again, you will forget your dream

46
Q

Other brain regions for sleep

A

Ventral part of frontal lobe: responsible for SWS stage 3 and 4

Reticular formation: arousal signals from sleep (how we wake up)

Hypothalamus: regulating transition between sleep stages and physiological sleep stages

47
Q

Common sense understanding of emotion

A

In reaction to a situation, we feel an emotion

48
Q

6 basic emotions

A

surprise, anger, fear, happiness, disgust, sadness

49
Q

James-Lange theory

A

The situation determines the physiological state, and the physiological state completely determines the emotion

50
Q

Supporting James Lange Theory

A

Facial Feedback hypothesis

physiological state: pencil making someone smile VS pencil making someone frown

People who were made to smile found things funny, others made to frown thought things were less funny

51
Q

Criticising James Lange’s theory

A

Our autonomic responses are relatively slow compared to speed of experiencing an emotion (therefore, how can physiological responses determine our emotion if they are slower to happen?)

If physiological responses determine emotion, we can test this by severing nerves from the visceral nerves to the brain which signal physiological changes
DID NOT SEE EMOTION CHANGES

Lots of our emotions (anger, happiness etc) have similar physiological responses. Injecting adrenaline did not change emotion, it changed only physiological state

52
Q

Cannon-Bard theory

A

Situation determines cognitive and physiological state independently.
To have an emotion about a situation, we need to have some thought process about it.

53
Q

Schacter and Singer two-factor theory

A

Situation determines our thoughts/appraisal and this creates our emotion. Physiological arousal determines the strength of emotion

54
Q

Schacter and Singer experiment

A

shows the link between how physiological state determines the intensity of emotion, but this is also limited/intertwined with cognitive appraisal

Groups placed into 2 situations (angry or happy)

Group A (adrenaline + told about injection)
Felt quite angry/happy due to physiological response, but dismissed this because they had positively interpreted/dismissed the bad parts of the situation

Group B (adrenaline + told about itchy eye balls)
Felt very angry/happy because of physiological response and because they had cognitively appraised negative sideffects

Group C (Adrenaline + not told anything)
Quite angry/happy due to physiological response and cognitive appraisal of anger provoking situation

Group D (no adrenaline + not told anything)
Neutral (shows that physiological state determines level of emotion)

55
Q

Dutton and Aaron’s two bridge study

A

higher physiological response = higher attraction

how we can mistakenly experience an emotion and get our cognitive appraisal wrong because of our physiological response

56
Q

Autonomic nervous system response to stress influencing emotion

A

Sympathetic nervous system:
Neural activation of adrenal medulla (hypothalamus activates adrenal medulla by synaptic transmission of signal)

Anterior Pituitary: Endocrine communication (diffuses across body, is slower than neural communication)
Hypothalamus releases Adrenocorticotropin releasing factor into bloodstream which reaches pituitary gland. Pituitary gland releases adrenocorticotropic hormone into bloodstream and this activates adrenal cortex (releasing cortisol)

57
Q

Aphasia

A

Disorders where language is not working

Types of aphasia:

Paraphasia: substitution of one word for another (mistake)

Neologism: making a new word that doesn’t make sense

Nonfluent speech

58
Q

Impairments related to aphasia

A

Agraphia/dysgraphia: inability/impairment of writing

Alexia/Dyslexia: inability/impairment of reading

59
Q

Language

A
  • Phonemes: smallest unit of sound that makes a difference to meaning (c-a-t)
  • Morpheme: smallest unit of language that has meaning (water, s, -ing)
  • Semantics: meanings of words
  • Syntax: how words are combined to construct phrases
60
Q

Precursor to Wernicke-Geshwind Model of language

A

Speech production issues: Broca’s area (lower left frontal lobe)
‘tan could understand what people were saying but could not say anything back’

Comprehension issues: Wernicke’s area (superior temporal gyrus in left hemisphere, posterior to primary auditory cortex)
‘patients could produce speech, but it wasn’t able to be understood’

61
Q

Licht Heim’s house

A

Could have damage to either areas used for speech production, comprehension, or conceptual parts of language

Auditory word form area: when we hear sounds, there is a part of our brain that recognises those and what they represent

Motor/spoken word form area: when we want to produce them as a spoken form

Wernicke’s patients: disruption to area which translates sound into recognising words (comprehension)

Broca’s patients: disruption to area where we hold motor plan for how to produce speech

62
Q

Wernicke-Geschwind model of language

A

Speaking a heard word:
1. primary auditory cortex (analysing the sounds)
2. Wernicke’s area: we hold the auditory word form and analyse it (we recognise those sounds as a word)
3. Transfer this info from Wernicke’s area to Broca’s area by arcuate fasciculus
4. Broca’s area holds motor plan associated with saying the word and sends this to motor cortex
5. Motor cortex implements plan (activates tongue muscles etc)

Speaking a written word:
1. Visual cortex: analysing the raw image
2. Angular gyrus: decodes image info to recognise visual form of word
3. Sends that info to Wernicke’s area which translates written form into auditory form
4. Wernicke’s area: sends that info to Broca’s area via arcuate fasciculus
5. Broca’s area: formulates motor plan to say the word and sends this to motor cortex
5. Motor cortex implements plan

63
Q

Broca’s aphasia

A

Being able to understand what people are saying, but not able to communicate back/communicating slowly

Broca’s area: anterior to portion of motor cortex controlling muscles in speech production (tongue etc)

Telegraphic speech: containing only most essential words for communication

Anomia: inability to come up with desired word

Preservation: repeating words they are capable of saying

Automatic speech: like tourettes

Hemiplegia: right sided paralysis due to damage of left frontal area which is near motor cortex (broca’s area) controlling right side of body

64
Q

Wernicke’s aphasia

A

Inability to comprehend speech from others and yourself, but having fluent speech

Wernicke’s area: left temporal lobe where we hold auditory word form area

Semantic paraphasia: unintended words which relates to intended meaning

Neologisms: creating novel words, putting 2 random sounds together

Circumlocutory speech: talk around concept rather than naming/identifying it

Do not have insight into their language difficulties

65
Q

Conduction aphasia

A

Disrupt transfer of info from Wernicke’s to Broca’s area (See licht heim’s model)

Retains typical speech comprehensions and speech productions

- Non-meaningful words are impossible to repeat because we don’t have any other mental representation of that word (no concept of that word)

The info between Wernicke and Broca’s area can’t go through pathway, but we can take a detour through the conceptual area (where meanings are applied to words)

Go from auditory representation of word to a visual representation, and then activate our speech form by using the visual representation

  1. Wernicke’s area: we recognise that sound ‘bicycle’ as being a word
  2. Transfer this info to the conceptual area and activate a visual representation of what a bicycle is
  3. Transfer this to Broca’s area which will trigger motor production of the word
66
Q

Higher order cognition (AKA executive functions)

A

Planning, problem solving, co-ordination of multiple thinking skills

Frontal lobe responsible for executive functions

67
Q

Types of executive functions

A

Inhibitory control: stops us from doing something automatic

Cognitive flexibility: flexible switching between tasks

Working memory: Multi-tasking

Hot executive function: real life scenarios (how do we use executive functioning when we have emotion and social influences)

Cold executive function: lab test scenarios

68
Q

Pre-frontal cortex - Dorsolateral prefrontal cortex

A

HIGHER ORDER COGNITIONS

Damage to this area causes: working memory, planning, task-setting, problem solving, attention, sequencing, preservation (doing something again even though its not working), cognitive flexibility

Tested by
FAS test: how many words can you come up with in a minute using 1 letter (detected repetitions in word repeating)

Digit span backwards: presented with series of digits, say one or 2 back from when you are (tests working memory)

Tower of London test: mirror other tower structure by only moving one block at a time (tests planning ability)

Wisconsin card slot test: tests cognitive flexibility and preservation by affirming the patient’s strategy of card sorting at first, but then changing the rules suddenly and causing them to change their strategy

Stroop test: sees how effective your inhibitory control is

69
Q

Prefrontal cortex - Orbitofrontal cortex

A

EMOTION AND SOCIAL INTERACTIONS

deficits involve: emotional liability/extremism, diminished social insight, socially inappropriate behaviour, difficulties with changing scenarios, lack of sensitivity, lack of empathy

FAS test: people may give socially inappropriate answers (and may not be aware of social construct against saying that word)

Bechara’s gambling task: control patients get emotionally aroused before choosing a risky deck, whereas damaged patients will get emotionally aroused after choosing a risky deck and losing alot (they dont have awareness of future good or bad outcomes)

70
Q

Prefrontal cortex- Mediofrontal cortex

A

MOTIVATION AND DRIVE

Deficits: apathy, akinesia (not a lot of moving), emotion difficulties, diminished verbal output

Lower reaction time: damage to mediofrontal cortex

71
Q

Acquired brain injury

A

all brain injuries after birth

72
Q

Conditions that can lead to ABI

A

Alzheimers/dementia

Parkinson’s

Multiple sclerosis

73
Q

Traumatic brain injury (TBI)

A

External causes of ABI (crashes, assault, sports, poisoning, alcohol, drug)

Internal causes of ABI (tumours, strokes)

Secondary effects of TBI (processes that brain goes from to heal itself, but actually worsens injury more): haemorrhage, intracranial pressure, brain swelling, epilepsy/seizure

74
Q

TBI classifications

A

Penetrating head injury: (projectiles, outside force etc)

Closed head injury: (brain accelerates and hits sides of the skull (frontal and temporal lobe highly vulnerable to injury because of bony ridges under skull plate) (pre-frontal cortex highly vulnerable due to its position in the brain, therefore motional and behavioural impacts are highly likely in TBI)

75
Q

Closed head injury

A

Coup: primary impact (bat hits head)

Contrecoup: secondary impact (brain hits other side of skull)

Contusions: bruising on the brain, internal bleeds, structural damage

Concussions: disturbance of consciousness and no evidence of structural damage (tearing of tissue around brain stem which impacts pons/consciousness)

76
Q

Stroke (CVA)

A

Haemorrhagic stroke: disruption of blood flow to brain due to bleeding in an artery

Aneurism: may cause haemorrhagic stroke due to ballooning of blood vessel which may explode

Ischaemic stroke: disruption of blood flow to brain due to blockage

Thrombotic stroke: thrombus (blood clot) blocks blood flow

Embolic stroke: fatty plaque/blood clot breaks away and flows to brain where it blocks artery and disrupts oxygen flow

77
Q

Classifications of TBI severity

A

GCS (motor operations, responses to stimuli)

LOC (duration of loss of consciousness)

PTA (Post-traumatic amnesia, period of confusion and disrupted memory function)

PSYCHOLOGY SEM 1 YR 1 (2 decks)

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