LAST MINUTE - clin psyc Flashcards

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1
Q

______ is the accumulation of fluid (.e.g, in the brain) that can lead to there being not enough space for the braint o swell into.

A

Oedema

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2
Q

Describe how the Glasgow Coma Scale is used to assess the depth of a patients coma. (describe how and what it measures)

A

The glasgow coma scale is a brief test of simple visual, verbal and motor abilities.

Visual - does the patient open their eyes? ranked from 1 (not at all) ->2 (to pain) ->3 (to speech)-> 4 (spontaneous)

Verbal - do they respond verbally? ranked from 1-5: none, incomprehensible, inappropriate, confused, orientated.

Motor - Do they respond to a motor command (e.g., can you move X) ranked from 1-6: none, extension, abnormal flexion, withdrawal, localises pain, obeys command

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3
Q

What GCS rating combined with Coma durations suggest Mild, Moderate and Severe traumatic brain injuries, respectively?

What level of disability are each of these categories predictive of?

A

MILD

  • GCS: greater than 13
  • Duration: less than 30 minutes
  • Predicts: good recovary

MODERATE

  • GCS: 9-12
  • Duration: less than 6 hours
  • Predicts: moderate disability

SEVERE

  • GCS: less than 8
  • Duration: greater than 6 hours after admission
  • Predicts: severe disability
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4
Q

What rating on the Glasgow Coma Scale is predictive of greater mortality?

A

A GCS score of less than 7.

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5
Q

At what score on the Glasgow Coma Scale is the unconsciousness considered to be a “Coma”?

A

less than or equal to 8.

however it is important to recognise that “coma” is a continuum from no coma -> shallow coma -> deep coma …and that people come out of coma gradual in stages.

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6
Q

Post-traumatic amnesia severity can be categorised based on it’s duration.

at what duration would PTA be considered:

  • very mild
  • mild
  • moderate
  • severe
  • very severe
  • extremely severe
A
  • very mild < 5 mins
  • mild 5-60 mins
  • moderate 1-24 hours
  • severe 1-7 days
  • very severe 1-4 weeks
  • extremely severe > 4 weeks
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7
Q

Another word for severe bleeding is_____

A

Haemorrhage

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8
Q

What are the four main complications of a closed head injury?

A
  1. Oedema (accumulation of fluid, not enough space for brain to swell into)
  2. Haemorrhage (bleeding) and resulting hematoma (accumulation of blood)
  3. Skull fractures (protrude into the brain and can result in infection)
  4. Post-traumatic epilepsy (due to scar tissue)
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9
Q

What are (or can be) the cognitive symptoms of traumatic head injury? (its neuropsychological profile)

A
  • Orientation
  • attention
  • memory
  • behavioural slowing
  • sensory function
  • verbal retrieval
  • executive functioning
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10
Q

What personality changes can result from traumatic brain injury?

A
  • Lack of initiative & loss of spontaneity
  • Temper outbursts & mood alterations
  • egocentricity
  • poor self-awarenss (of deficits)
  • deppression (usually after 6 months post-injury)
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11
Q

Describe the duration of loss of consciousness(LOC) post-traumatic amnesia (PTA) and ‘complaints’ consistent with a mild traumatic head injury (i.e., concussion)

A
  • LOC: less than or equal to 30 mins
  • PTA: less than or equal to 24 hours
  • Complaints: less than or equal to 3 months (changes in the brain are microscopic)
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12
Q

What are the common complaints of a mild traumatic head injury (i.e., a concussion)?

How long does it usually take complaints to emerge?

How long does recovary usually take?

A

PHYSICAL

  • Dizziness, headaches, noise sensitivity, vision (e.g., blurred)

COGNITIVE

  • Orientation (initial person/time/place), Attention (concentrating) and Memory

PERSONALITY

  • Patience/temper, anxiety and deppression.

Symptoms/complaints emerge a few days after injury (When people attempt to resume regular activity)

Recovary can take 3 months and symptoms tend to disappear gradually.

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13
Q

What is the timeline of recovery for traumatic brain injuries?

During what time period are the most recovery gains made?

A

Max level of recovery reached around 2 years post-THI

Most gains made during the first 6 months.

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14
Q

a _______ is when a temporary obstruction occurs in an artery resulting in temporary hypoxia.

is short lasting resulting in transient deficits.

A

Transient Ischemic Attack (TIA)

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15
Q

______ is when there is an permanent obstruction in a blood vessel resulting in prolonged hypoxia resulting in necrosis (i.e., an infarction)

A

Obstructive Ischemic Stroke

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16
Q

What are the symtoms of a Transient Ischemic Attack (TIA)?

A

Physical - dizziness

Cognitive - orientation, sensation & perception, language, motor skills (weakness)

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17
Q

_____is a Type of Obstructive Ischemic Stroke whereby plague forms elsewhere in the body and travels to the brain where it blocks a blood vessle

A

Embolic

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18
Q

_____is a Type of Obstructive Ischemic Stroke whereby fatty deposits built up in vessle walls block/narrow blood vessles in the brain (accident occurs over 30minutes)

A

Thrombotic

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19
Q

The space between the surgace of the brain and the skull is called the _______

A

subarachnoid space

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20
Q

_____ referes to inside the brain itself

A

Intracerebral

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21
Q

What are the common cognitive symptoms of a CVA?

A
  • Orientation - self, place, time
  • Attention -
  • Motor function - slowing, paralysis, unsteady, coordination
  • Executive function - trouble planning, organising, responding to novel situations
  • Memory - mostly STM (LTM usually alright) misplace things, getting lost, struggle to live independently - structure is important
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22
Q

What are the common cognitive symptoms of a CVA?

A
  • Orientation - self, place, time
  • Attention -
  • Motor function - slowing, paralysis, unsteady, coordination
  • Executive function - trouble planning, organising, responding to novel situations
  • Memory - mostly STM (LTM usually alright) misplace things, getting lost, struggle to live independently - structure is important
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23
Q

How do the symptoms of a left hemisphere stroke differ from those of a right hemisphere stroke?

(i.e., lateralisation)

A

for the 98% of people with left language lateralisation:

  • damage to the left hemisphere affects receptive and expressive language.
  • damage to the right hemisphere affects visual-spatial ability (perceptual, estimating distances between points)
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24
Q

What personality changes can result from a CVA?

(and the hemisphere where possible)

A
  • Depression (left hemisphere stroke)
  • Apathy/indifference (right hemisphere)[tone expression]
  • Euphoria (right hemisphere stroke)
  • Impulsiveness
  • Emotional lability - exagerrated or incongruent responses
  • Lack of initiation - not being able to start a behaviour
  • Perseveration - Not being able to stop a behaviour
  • Poor judgement - leading to inappropriate or dangerous behaviour
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25
Q

What are Lack of initiation and
Perseveration, respectively?

A
  1. Not being able to start a behaviour
  2. Not being able to stop a behaviour
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26
Q

What is the recovary timeline for CVAs?

When does most of the recovery occur?

A

Plateau at 6 months

Improve most rapidly for the first few weeks

(i.e., quicker initial recovery and quicker plateau than brain injury patients.)

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27
Q

what is “epilepsy”?

A

A cluster of symptoms

  • Recurring seizures (reversable alterations of consciousness) [ arousal alertness, awareness
  • Hyperventilation
  • Migraine
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28
Q

the ______ posits a negative linear relationship between age of brain lesion and outcome expectancy

A

Kennard Principle

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29
Q

_______ is not being able to start a behaviour

A

lack of initiation

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30
Q

_____ is not being able to stop a behaviour

A

perseveration

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31
Q

The first stage of a seizure where Auras occur is known as the _____

A

Prodromal phase

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32
Q

The second stage of a seizure where a person experiences a temporary change in consciousness is known as the ______

A

Ictal phase

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33
Q

The last stage of a seizure where a person regarins consciousness (minutes or hours later) is known as the ______

A

post-ictal phase

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34
Q

strange pre-seizure symptoms that occur in the prodromol phase such as dizzy, nauseous, metallic taste, smells, mood changes, deja-vu, stomach butterflies are know as______

A

AURAs

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35
Q

Seizures were the whole brain is involved/affected are _______ seizures

A

Generalised

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36
Q

Seizures were only part of the brain is involved/affected are _______ seizures

A

partial (focal)

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37
Q

What type of genealised seizure involves a person letting out a cry, crumpling, face goes blue, stop breathing, tense/rigid —-> follow by approx 30 secs on rythmic jerking?

A

Grand mal seizure

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38
Q

in the _____ phase of a grand mal seizure a person might let out a cry, crumple, their face goes blue, they stop breating and they go tense/rigid for about 30seconds

A

Tonic

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39
Q

in the _____ phase of a grand mal seizure a person has rythmic jerking of the limbs for approx 30 seconds.

A

Clonic

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40
Q

partial seizures with one mode of expression are called ______

A

simple seizures.

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41
Q

partial seizures involving an entire lobe or a number of brain areas are known as_______

A

Complex partial seizures

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42
Q

partial seizures involving the motor cortex are know are_____

A

Jacksonian/marchign seizures.

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43
Q

_____ involve repeatedly doing the same behaviour (i.e., ‘stuck’) and feature in complex partial seizures.

A

Automatisms

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44
Q

Seizures of the motor cortex. That start with muscle contractions in just one area (e.g., moving one finger) then the seizure progresses across the motor cortex, are known as_______

A

Jacksonian/marching seizures

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45
Q

The ________ is a test done prior to surgery for epepilepsy whereby a barbituate is injected at the base of the brain which causes 6-8 minutes of half-brain paralysis.

This enables the neuropsychologist to ensure that the other side of the brain can compensate, thus it is highly useful for partial sezures, specifically temporal lobe seizures.

A

WADA

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46
Q

What is the neuropsychological profile of epilepsy? (cognitive and personality symptoms)

A

Cogntive symptoms

  • attention
  • memory and learning

Personality symptoms

Epilepsy ->

Reduced quality of life -> : limitations in driving, swimming, jobs, reduced social interaction (no late nights or alcohol.

**Personality changes: **anxiety, deppression, tension, stress, psychotic. (high than in the general population)

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47
Q

Personality are most common in what kind of epilepsy?

A
  • Most common in temporal lobe epilepsy (mood, detail obsessed)
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48
Q

What are the treatments for epilepsy?

A
  • Anticonvulsant medication
  • Surgical procedures
  • Behavioural management
  • Seizure control
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49
Q

Split-brain surgery, whereby the corpus-collosom is cut is called a _______

A

Commissurotomy

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50
Q

Recognising the signs of an impending seizure and counteracting them

e.g., a patient with a specific smell aura, may purposefully smell something different.

A patient with a specific taste aura, may purposefully eat somehing pleasant

this is an example of ______

A

Seizure control

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51
Q

An abnormal groth of brain tissue is called a?

A

Neoplasm (i.e., brain tumour)

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52
Q

What role does the Neuropsychologist have in Evaluation in the case of epilepsy?

A
  • Functional asessment during WADA test (brief assessment of language and memory function)
  • Determine prescense and extent of cognitive & personality disturbances
  • Rudimentry assessment of cerebral organisation for speech.
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53
Q

a tumour that is spread out, invades and destroys other areas of the brain, consumes healthy tissue has an ______nature

A

Infiltating

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54
Q

a tumour oninvading that is an encapsulated growth, growing within itself, does NOT ‘take-over’ has a ______ nature

A

non-infiltrating

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55
Q

a tumours rate of growth and the degree of symptoms it is casuing is reffered to as its _____

A

Malignancy

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56
Q

A Secondary brain tumour” whereby tumour ceels brak of from a primary cancer elsewhere in the body (e.g., lungs) and travel through the blood to the brain is reffered to as having a ______ origin

A

Metastatic

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57
Q

What is the ‘malignancy’ of a tumour? and how is it graded?

A

The tumours rate of growth and the degree of symptoms it is causing

it is graded from 1-4

  1. Slow growth, minimal symptoms
  2. low-Intermediate growth, low-moderate symptoms
  3. Intermediate growth, moderate symptoms
  4. Fast growth, severe symptoms
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58
Q

How does the damages caused by an infiltrating tumour differ from that caused by a non-infiltrating tumour?

A
  • Infiltrating tumours - invade and destroy healthy brain tissue, directly damaging the brain tissues.
  • Non-infiltrating tumours - are encapsulated, but as they grow they cause intracranial pressure (ICP) which displacees and compresses the healthy brain tissue causing damage.
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59
Q

What are the (behavioural/sickness) symptoms of a brain tumour?

A
  • Headaches (pressure as tumour grows)
  • Nausea and vomiting
  • Seizures
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60
Q

How is a brain tumour diagnosed?

A

Brain imaging techniques (both are similar, but MRI is more detailed) - locates tumour

  1. CT - visualise structure of cells
  2. MRI - differentiate between brain cells and tumour cells

Brain biopsy - determines the type of tumour

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61
Q

______ is a procedure by which a neuropsychologist works out what areas around a tumour ‘do’ and thus what will be affected by the removal of a tumour and nearby tissues. i.e., mapping out brain functions.

It helps the surgeon determine the “balancing act” between removing tumour cells and protecting brain cells. If the area contains important function, the surgeon may choose to be more conservative (at the risk of tumour reoccurance). Surgery is often followed by radiation.

the process:

Local anestetic and the skull is opened, exposing the brain
Low voltage electrode directly stimulates the brain area
patient responds e.g., touch motor cotex and they move their hand, or they are asked to count etc.
Because, for example, a motor cortex tumour could cause motor trouble and a tumour in the basal ganglia could cause tremours.

A

Cortical stimulation

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62
Q
A
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63
Q

What role does the neuropsychologist have in evaluation in the case of brain tumour (and surgery/treatment)?

A
  1. Evaluate baseline (which areas are most affected by the tumour)
  2. Patient has surgery or treatment
  3. Follow-up (hopefully documents improvement)
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64
Q

Risk factors for cerebrovascular disorders include:

A. gender

B. High cholesterol

C. History of traumatic head injury

D. Both A and B

A

D: both A and B (Gender and High cholesterol)

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65
Q

The cognitive symptoms associated with temporal love epilepsy include…

A. Visual-spatial deficits

B. Memory impairments

C. Executive dysfunction

D. All of the above

A

B. Memory impairments

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66
Q

The rey figure test is an assessment instrument used to measure the cogntive functioning of ______

A

Visual-spatial organisation

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67
Q

What is the purpose of neuropsychological evaluation?

A
  • Profile patient strengths and weaknesses
  • Differentiate between functional and organic disorder
  • Document impact of brain dysfunction on a patients life
  • Monitor progress in rehabilitation
  • Disability determination for froensic/legal purposes.
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68
Q

What is reliability?

What are the 4 types of reliability?

A

Reliability: the stability/dependability/consistency of a test on repeated measures of the same person. Includes:

  • Test-retest reliability - consistency between scores of an individual measured more than once.
  • Inter-rater reliability - reliability between different people’s use of the measure to score the same individual
  • Split-half reliability - the correlation between two halfs of a test
  • Internal reliability/consistency - the degree to which items of a scale measure the same thing, also known as ‘cronbach’s alpha)
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69
Q

What is validity?

What are the 3 types of validity?

A

A test is valid when it measures what it purports to measure. The validity of a test is the meanifulness of specific inference made from the test scores.

An unreliable test cannot be valid, but a non-valid test can be reliable.

  • Construct validity - does the test score measure the abstract psychological charactersitic or construct of interest (e.g memory or intelligence etc.)
  • Content validity - do the items or tasks that make up your test make conceptual sense. Various items of teh test should correspond to the behavior te test is designed to measure or predict.
  • Criterion validity - demonstrates that scores relate systematicaly to one or more outcome criteria. has two components:
  1. Concurrent validity - relates to outcomes now (important for testing capacities now)
  2. Predictive validity - relates to outcomes in the future (e.g predicting improvements or decline in recovary)
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70
Q

Neuropsychological testing focuses on what functional areas? (from the most basic to the most complex)

A
  1. Orientation
  2. Sensation/perception
  3. Attention
  4. Motor skills
  5. Language
  6. Visuospatial
  7. Memory
  8. Executive functioning (abstract reasoning/conceptualisation, emotional/psychological distress, activities of daily living)
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71
Q

What part of the brain is (predominately) responsible for orientation?

Where is it in the brain?

A

Reticular formation.

The reticular formation is a group of nerve fibers located inside the brainstem.

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72
Q

The Galveston Orientation and Amnesia Test (GOAT) is used to assess____?

A

Orientation and amensia (inc awareness)

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73
Q

______is the processing and intepretation of sensory input

A

Perception

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74
Q

______is the stimulation of sensory organs (touch, vision, hearing, taste, smell)

A

Sensation

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75
Q

Halstead-Reiten Neuropsychological Battery (visual, auditory & tactile modalities) is used to assess?

A

Perception/intepretation

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76
Q

Where are the two parts of the brain that deal with TOUCH sensation, what are they called and what do they do?

A
  1. Primary somatosensory cortex - basic awareness of touch - in the parietal lobee
  2. Secondary system - Intepretation - parietal lobe

The primary somatosensory cortex (SI) is across the central sulcus and behind the primary motor cortex configured to generally correspond with the arrangement of nearby motor cells related to specific body parts. The area includes gray matter along the central gyrus and its extension into the postcentral gyrus.

Goes across both brain hemispheres.

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77
Q

Where are the two parts of the brain that deal with VISION sensation, what are they called and what do they do?

A
  1. Primary visual cortex - the occipital lobe
  2. Secondary area of the visual cortex - two systems: ‘what’ system (faces, objects), ‘where’ system (where in space) - the occupital lobe

“The visual area known as V1, striate cortex, or (primary visual cortex, Brodmann area 17) is located on the calcarine sulcus deep within the inside folds of the occipital lobe.”

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78
Q

Where are the three ares of the brain that deal with HEARING sensation, what are they called and what do they do?

A
  1. Primary auditory cortex - frequency volume length
  2. Secondary area 1 - Wernickes area (Temporal lobe) - Understanding speech
  3. Secondary area 2 - Brocha’s area (Frontal lobe) - produce speech
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79
Q

_______ attention is paying attention ot something over a prolonger period

A

sustained

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80
Q

_____attention is paying attention to more than one thing at a time.

A

Selective

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81
Q

What areas of the brain are involved in attention/concentration?

A

Frontal lobe and Parietal Lobe

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82
Q

What does the Symbol Digit Modalities Test i.e., SDMT (see picture) assess?

A

Attention/concentration

specifically assesses: complex scanning, visual tracking and sustained attention

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83
Q

What is the D2 test used to assess?

A

test of selection attention

measures processing speed, rule compliance and quality of performance; allowing estimation of individual attention and concetration performance.

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84
Q

Getting a person to attend to various verbal stimuli and then repeat them, becoming progressively more complex. e.g repeating numbers (589, 9275, 71632) and then also do it backwards. is an assessment of ________

A

Attention span

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85
Q

_____ is the inability to perform purposeful sequences of motor behaviours.

A

Apraxia

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86
Q

the _______involves commands regarding shapes in a picture e.g show me a pink shape, show me a blue square, show me a small blue shape,show me the green sqaure etc.) and is a test of ________

A

Token test; receptive language

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87
Q

What do the following subtests of the Halstead-Reitan Neuropsychological Battery assess?

Finger-tapping test - tap index finger as fast as possible.
Grip strength test - measure with a hand-dynamometer - 3 goes with each hand averaged.

A

Motor skills

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88
Q

What aspects of motor function is dealt with by the frontal lobe and basal ganglia/cerebellum respectively?

A

Frontal lobe = Planning/sequencing

Basal ganglia/cerebellum = coordination and balance

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89
Q

What part of the brain handles understanding language? (i.e., receptive language) and where is it on the brain?

A

Wernikes area

Traditionally thought to be located posterior section of the superior temporal gyrus (STG) in the dominant cerebral hemisphere (which is the left hemisphere in about 97% of people).

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90
Q

Which hemisphere is broca’s area and Wernickes area situatied in?

A

The left hemisphere in about 97% of people, but it is in the right hemisphere for some people.

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91
Q

What part of the brain handles producing language? (i.e., expressive language) and where is it on the brain?

A

Broca’s area

Broca’s area is a region in the frontal lobe of the left hemisphere

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92
Q

the _____ involves come up with words beginning with # (a letter) letter in 1-minutes, must be more than four letters long and not names or partial repitions. and is a test of _____.

A

Controlled Oral Word Association test (COWA); Expressive language

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93
Q

the __________ involves simple line drawing of common objects, if they can’t name what the object is they are given a stimulus (e.g for ‘seahore’ might say ‘it’s an ocean creature’). if they still have trouble they are given a phonetic cue (e.g it starts with a ‘c’ sound) and is used to assess_______

A

Boston Naming Test; Language

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94
Q

Why are the letters F, A and S often used in the Controlled Oral Word Association (COWA) test

A

F = lowest digital frequency

A = vowel

S = Highest digital frequency

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95
Q

_____ language describes the patients ability to comprehend simple spoken commands (e.g., ‘say hello’)

A

Receptive

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96
Q

____ language is vocabulary knowledge and recognition of concepts and objects (e.g., please tell me wheat ‘happiness’ means or ‘make up a sentance using the word ‘vacation’)

A

Expressive

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97
Q

____ is Deficits in the motor component of writing

A

Dysgraphia

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98
Q

The clock drawing test, Rey figure test and directional skills/mazes/motor-free construction tasks; and facial recognition are used to assess _____

A

Visuo-spatial organisation

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99
Q

What is ‘visual-spatial organisation’ and what factors does it include?

A

Involes a range of cognitive processes e.g., map reading, route finding, visual perception, constructional ability & facial expressions)

  • Construction
  • Route Finding
  • Spatial orientation
  • Facial recognition
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100
Q

_______ is The intentional production of false or grossly exaggerated physical or psychological symptoms, motivated by external incentives such as avoiding military duty, avoiding work, obtaining financial compensation, evading criminal procecution, or obtaining drugs.

A

Malingering

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101
Q

the ________ apprach to neuropsychological intepretation relis on perfroming a broad set series of standardised tests

A

standard battery approach

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102
Q

the ________ is the idea that the neuropsychologist should adapt each examination to the individual patient rather than use a standard battery of tests. The neuropsychologist selects the tests and procedures for each examination, using hypotheses he or she has made from impressions of the patient and from information available about the patient.

A

Process approach

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103
Q

memory for factual information is also known as _____

A

Explicit/declarative memory

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104
Q

What are the advantages of the standard Battery approach to neuropsychological intepretation?

A
  • Comprehensive evaluation of abilities
  • Objective interpretation based on normative data
  • Facilitates teaching because of standard rules/norms
  • Useful for empirical studies
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105
Q

What are the disadvantages of the standard Battery approach to neuropsychological intepretation?

A
  • Time demanding and labor intensive
  • Tests only as good as standardisation
  • Relatively infelxible approach to testing
  • Scores may not reflect a single cogitive process
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106
Q

What are the advantages of the ‘Process Approach’ to neuropsychological intepretation?

A
  • Acknowledges the individuality of the patient
  • Examination focuses on most important deficits
  • Emphasizes how a task is failed or solved
  • Useful for clinical case studies
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107
Q

What are the disadvantages of the ‘Process Approach’ to neuropsychological intepretation?

A
  • Test procedures may be biased by clinician
  • Opinion of the clinician is subjective
  • Difficult to teach, because it requires experience
  • Does not lend itself to large-scale research
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108
Q

What type of memory deals with action or “doing” memory?

A

Implicit/procedural

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109
Q

What 3 main areas of the brain are involved in memory? and what aspects of memory are they associated with?

Where in the brain is the the basal ganglia and the cerebellum?

A
  1. Hippocampus (middle of the temporal lobe) - encoding and cognitive maos
  2. Basal Gaglia (mid-brain) - motor memory
  3. Cerebellum - learning of procedural memory and motor learning
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110
Q

The Wechsler memory scale and
Rey Auditory Verbal Learning test are used to test what?

A

MEMORY

WMS: verbal, visual, STM, LTM, serial recall, free recall, recognition

RAVL: Immediate memory, verbal memory, suceptability to interference, recognition memory)

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111
Q

What is the trail making test used to asses?

A

Executive functioning

Specifically: mental flexibility

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112
Q

What is the winconsin card sorting test used to assess?

A

Executive Functioning - shift between sorting categories and ignore irrelevant information

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113
Q

What is the tower of london task used to assess?

A

Executive functioning - specifically plannin and problem solving.

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114
Q

a _________ involves comparing an individual’s test scores to test norms

A

normative comparson standard

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115
Q

What is the WAIS and what is it used to test?

A

Wechsler Adult Intelligence Scale

Used to assess Intelligence

6 verbal scales and 5 performance scales

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116
Q

Is factual information or learning experience factors (culture incl.) fluid or crystallised intelligence?

A

Crystallised

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117
Q

What is the purpose of ADLs (Adaptiving Living or Behaviour-Adaptive tests)?

A

gives an assessment of activities of daily living (e.g., bathing, grooming, feeding), that enables recommendations about care facilities or helps determine compensation litigation.

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118
Q

What does the “Category” subtest of the Halstead-Reiten Neuropsychological battery assess?

A

Abstract reasoning

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119
Q

What does the “seashore rhyming test” subtest of the Halstead-Reiten Neuropsychological battery assess?

A

Auditory perception

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120
Q

What does the “speech-sounds perception test” subtest of the Halstead-Reiten Neuropsychological battery assess?

A

Verbal Ability

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121
Q

What do the “grip-strength” and “finger tapping” subtest of the Halstead-Reiten Neuropsychological battery assess?

A

Motor Skills

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122
Q

What does the “Tactile Perfromance” subtest of the Halstead-Reiten Neuropsychological battery assess?

A

Tactile Memory

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123
Q

What does the “sensory-perceptual examination” subtest of the Halstead-Reiten Neuropsychological battery assess?

A

Sensory and perceptual functions

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124
Q

What does the “aphasia examination” subtest of the Halstead-Reiten Neuropsychological battery assess?

A

Language ability

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125
Q

_________involes testing a patient at multiple time-points (e.g every few weeks) and comparing the results.

When assessing decline (e.g., dementia) or improvement

A

Individual compariosn (standard)

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126
Q

_____ is a type of maligering were one pretends to be worse off

A

simulation

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127
Q

_____ is a type of maligering were one pretends to be better off

A

dissimulation

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128
Q

what is the Rey 15 item memory test used to detect?

A

Malingering

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129
Q

The biological repair of neurons is called ____

A

Neuronal restitution

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130
Q

When function is impaired but not lost and the usual ‘way of doing things’ is restored it is reffered to as ____

A

Psychological restitution.

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131
Q

Compensation with other brain areas is reffered to as _____

A

Neuronal substitution.

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132
Q

Use of adaptive stratergies/compensatory stratergies is reffered to as _______

A

Psychological substitution

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133
Q

_______ is the processes of restitution and substitution applied to neuropsychological treatment

A

Cognitive remediation

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134
Q
A
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135
Q

What does the neuropsychologist do DURING the rehabilitation process?

A

Conducts regular follow-up assessments

  • Monitor patient progress
  • Evaluate effectiveness of treatment program

Counsels caregivers and family members

  • Effects of brain damage on behaviour
  • stratergies to cope with cognitive and behavioural deficits
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136
Q

Becks Depression Inventory (BDI)

What function does it test?

What brain structures does it asses?

What clinical population is it used for?

A

Measures deppression (both cognitive-affective and somatic symptoms)

Assesses personality changes i.e., an indirect relationship to brain injury/disability

any population

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137
Q

Deppression, Anxiety and Stress Scales (DASS)

What function does it test?

What brain structures does it asses?

What clinical population is it used for?

A

Measures deppression, Anxiety & stress (long form DASS [42 items], short for DASS-21)

Assesses personality changes i.e., an indirect reaction to brain injury/diability

Any population

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138
Q

Hooper Visual Organisation Test

What function does it test?

What brain structures does it asses?

What clinical population is it used for?

What does the test involve?

A

Measures ability to mentaly manipulate and reintegrate visual imformation

Parietal lobe

Dementia (often used for elderly driving assessment), stroke, brain injury

Patient identifies 30 objects represented in line drawings as puzzle pieces - what would the picture be if the pieces were back together

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139
Q

Judgement of Line Orientation

What function does it test?

What brain structures does it asses?

What clinical population is it used for?

What does the test involve?

A

Measures spatial perception, orientation and visuospatial judgement

Visual cortex, frontal lobe

Traumatic brain injury, dementia (alzheimers, turner syndrome, parkinsons, left visual neglect)

Judging the orientation of lines!

140
Q

National Adult Reading Test (NART)

What function does it test?

What brain structures does it asses?

What clinical population is it used for?

What does the test involve?

A

Test of premorbid intelligence functioning (level of cognitive functioning before brain injury)

N/A - but damage to certain areas of the brain will mean a person is unable to pronounce words (e.g., expressive language - broca’s area)

Anyone for who cognitive decline is suspected (dementias or brain injuries)

A list of words that have an unusual pronounciation. the person needs to be familiar with the words to be able to pronounce them)

141
Q

Rey Auditory Verbal Learning Test (RAVL)

What function does it test?

What brain structures does it asses?

What clinical population is it used for?

What does the test involve?

A

Test of verbal learning, immediate memory, recognition and susceptibility to inteference, recognition.

Hippocampus

Individuals suspected of memory dysfunction (Dementias or brain injury)

Immediate memory (A-list x1) -> verbal memory (A-list x4) -> Immediate memory (B-list x1) -> 20-minutes of non-related tests -> LTM/delayed memory (A-list x1) -> Recognition (A+B+20 similar words)

142
Q

Rey Complex Figure

What function does it test?

What brain structures does it asses?

What clinical population is it used for?

What does the test involve?

A

Measure of visuospatial construction and visuospatial memory (also assesses planning, organisation and fine motor skills)

Parietal lobe

Brain injury, dementia, and to assess some developmental learning deficits

Examinees are asked to reproduce a complicated line drawing, first by copying it, and then from memory.

143
Q

Token Test

What function does it test?

What brain structures does it asses?

What clinical population is it used for?

What does the test involve?

A

Measures receptive language

Wernickes area

Brain injury, aphasia, and certain language and learning disabilities.

series of commands regarding plastic shapes of different shape, size and colour - increasing complexity (e.g., touch a square, touch a yellow square, touch a yellow small square, touch a yellow small square and a small blue circle)

144
Q

Wisconsin Card Sorting Test

What function does it test?

What brain structures does it asses?

What clinical population is it used for?

What does the test involve?

A

Measures ability to shift categories and inhibit irrelevant responses. (executive functioning)

Frontal lobe

used in patients with acquired brain injury, dementias and mental illness

  • 4 face up cards + participant response ards with similar shapes, colours and numbers (of shapes).
  • Patients sort the cards either by colour, shape or number - but the examiner does NOT TELL THE P THE ‘RULE’ - they are told “right” or “wrong” for each sort attempt, when they do the right sort x10, the rule is changed.
145
Q

Grip Strength Test

What function does it test?

What brain structures does it asses?

What clinical population is it used for?

What does the test involve?

A

Assesses lataralised cortical impairment

Motor cortex

Brain injury

Use of a hand-dynamometer

146
Q

What neurospychological tests would you use to assess depression, anxiety and stress? (personality changes)

A

Depression, Anxiety and Stress Scales (DASS)

Beck Deppression Inventory (BDI)

147
Q

What test would you use to assess expressive language and Broca’s area?

A

Boston Naming Test

148
Q

What test would you use to measure the ability to mentally manipulate and reintegrate visual information?

A

Hooper Visual Organisation test

149
Q

What test would you use to measure spatial perspection, orientation and visuospatial judgement?

A

Judgement of Line Orientation

150
Q

What test would you use to assess premorbid intellectual functioning?

A

National Adult Reading Test (NART)

151
Q

What test would you use to assess verbal learning, immediate memory, recognition and susceptibility o inteference?

A

Rey Auditory Verbal Learning Test (RAVL)

152
Q

What test would you use to assess visuospatial construction and visuospatial memory (also planning organisation and fine motor skills)?

A

Rey Complex Figure

153
Q

What test would you use to assess ability to shift categories and inhibit irrelevant responses?

A

Wisconsin Card Sorting Test

154
Q

What test would you use to assess receptive language?

A

Token Test

155
Q

What test would you use to assess lataralised cortical impairment?

A

Grip strength test

156
Q

What test would you use to assess excutive functioning/mental flexibility?

A

Trail-making test

157
Q

What test would you use to assess planning and problem solving (executive functioning)?

A

Tower of London Task

158
Q

According to the Diagnostic and Statistical Manual of mental disorders what is the definition of a mental disorder?

(2 key components).

A
  1. Clinically significant disturbances
  2. Usually associated with significant distress or disability

“A set of symptoms (abnormal thoughts, feelings and behaviours) that are sufficiently ‘sever’ to cause significant A. distress and/or B. disability (impairment/limitations)”

159
Q

A psychological disorder is NOT…..

A
  • Eccentric behaviour
  • Violation of social codes
  • Temporary and expectable distress/disturbances in response to negative experience (e.g., grief)
160
Q

In terms of mental disorders, what does “qualitatively” different mean?

A

Radically different/bizzare

e.g.,

Psychologist: “ have you been nervous or tense lately?”

Patient: “No, I’ve got a head of lettuce”

161
Q

In terms of mental disorders, what does “quantitatively different” mean?

A

Differences in quantity/degree/frequency/intensity of things that everyday people feel/experience.

e.g., a fear of spiders VS. a phobia of spiders (real impact)

162
Q

What is the lifetime prevalence of Panic disorder?

A

5%

163
Q

What is the lifetime prevalence of specific phobia?

A

12%

164
Q

What is the lifetime prevalence of substance use?

A

14%

165
Q

What is the lifetime prevalence of Major deppression disorder?

A

16%

166
Q

What is the lifetime prevalence of any anxiety disorder?

A

29%

167
Q

what are the 7 major disorder groupings in the DSM?

A
  1. Neurodevelopmental disorders (ADD, autism)
  2. Bipolar and related disorders (mania)
  3. Deppressive disorder (MDD)
  4. Anxiety disorders (Panic)
  5. Feeding and eating disorders (Anorexia)
  6. Schizophrenia spectrum and other psychotic disorders
  7. Neurocognitive disorders (Cognitive function - alzheimers/parkinsons)
168
Q

What are the three main formal assessment technique?

A
  • Structured interviews
  • Questionaires
  • Daily diaries
169
Q

What are the properties of a structured interview?

A

A structured interview involving Initial & probe/follow-up questions.

Follows a manual including:

  • Glossary of terms - definitions
  • Standardised scoring
  • Guide to intepretations

Yields information about frequency, nature and (often) severity of presenting problems.

170
Q

What are questionaire inventories?

A

Self-report with close ended questions

171
Q

How does good clinical research use structured interviews and questionaires?

A

Confirms the diagnosis of participants using structured interviews.

Questionaires are usefull as screening measures and often appropriate for monitoring progress in clinical practice & research. (but they do not provide specific details about the nature, occurance or impact of client’s problems.

172
Q

Why are theories important?

A

They inform treatment decisions - because if we understand why a problem occurs, we’re in a better position to try and solve it.

Theory - > Therapy

173
Q

What is a theory (of a disorder)?

A

Explanation for the development & maintenance of a disorder.

174
Q

A disroder reated/cause by therapy is known as a _____disorder?

A

Iatrogenic

175
Q
A
176
Q

What is the trauma model of Dissociative Identity Disorder?

A

DID develops as a way of coping with overwhelming abuse in childhood, particularly if abuse occurs before age 5

  • Dissociation (separating memories from awareness) and amnesia (repression of memories)
  • Differen alters ‘own’ different threatening emotional states (e.g., fear, rage) and different memories, so the primary personality is protected and not aware of them
  • high hypnotisability facilitates this.
177
Q

What are some predictors of dissociative identity disorder?

A

Sexual and physical abuse during childhood; high scores hypnotisability and dissociative capacity; PTSD, self-mutilation, suicide, aggressive behaviour; numerous other DSM-IV disorder.

178
Q

are there sex differences in the occurance of dissociative identity disorder?

A

Large number of studies suggest that it is more common in women female:male = 3:1–>9:1

DSM-5 now says similar rates in women and men - but this is based on one small community study (bad!)

179
Q

schizophrenia, other psychotic disorders, bipolar disorder with rapid cycling, anxiety disorder, somatization disorders, personality disorders, malingering and factitious disorder are ____________for dissociative identity disorder

A

Differential diagnosis (i.e., other disorders with which DID could be confused with/misdiagnosed)

180
Q

How did the DSM-4 and DSM-5 criteria for dissociative identity disorder differ?

A
  • DSM-4 required two or more distinct identities or personality states, that take over behaviour.
  • DSM-5 more GENERAL, just a disruption of identity.
181
Q

What is the DSM-5 criteria for Dissociative Identity Disorder?

A
  • DSM-5 more GENERAL,

A. disruption of identity characterized by two or more distinct personality states (like possessions), alterations in affect, consciousness, memory, perception, cognition and/or sensory functioning.

B. gaps in recall of everyday events/important personal info

C. clinically significant distress or impairment.

D. disturbance not part of culture/religion.

182
Q

Client ______ need to be considered when selecting the appropriate treatment for major depressive disorder.

A

preferences

183
Q

What is the best treatment for major depressive disorder?

A

Best?

  • CT = BT
  • BT = CBT
  • CBT(60=70%) > drug (40-60%),

high placebo-drug effect (30%). Medication does not require skill & might make CBT easier, but drugs have a high dropout rate.

184
Q

Cognitive therapy for major depressive disorder may include ______ which involve testing a prediction that a bad thing will happened when X happens.

A

Behavioural experiments

185
Q

outline cognitive therapy as a treatment of Major depressive disorder.

A
  • AIM: teach clients to identify and challenge/refute irrational cognitions.
  • clients ask themself questions regarding the evidence, alternative intepretations and logical errors of their beliefs/cognitions.

reinterpretation and thought diary.

186
Q

_____ is a treatment for major depressive disorder that is designed to increase activity and positive consequences and increase skills in gaining reinforcement and reducing avoidance

COMPONENTs

pleasant activities (Reinforcement potential)
tasks that need to be done
pre-agreed
self-monitored (e.g., diary)
Graded
may also include skill training

A

Activity scheduling

187
Q

What are the properties of a structured interview?

A

A structured interview involving Initial & probe/follow-up questions.

Follows a manual including:

  • Glossary of terms - definitions
  • Standardised scoring
  • Guide to intepretations

Yields information about frequency, nature and (often) severity of presenting problems.

188
Q

What is a theory (of a disorder)?

A

Explanation for the development & maintenance of a disorder.

189
Q

_______ can be said to have occured/be occuring when anxiety diminishes with ongoing exposure to a feared stimulus.

A

Habituation

190
Q

How is systematci desensitation different to modern exposure theory?

A

Involves relaxation techniques that are not present in exposure therapy.

it tries to link a CD with a state incompatible with the CR, namely, relaxation.

191
Q
A
192
Q

What is the main premise of Operant Conditions?

A

Many behaviours depend on their consequences.

Positive consequences -> repeat behaviour

Negative consequences -> do not repeat behaviour

193
Q

According to operant conditioning, what types of consequences maintain or increase a behaviour?

Give an example using the example of a phobia of birds

A
  • Positive Reinforcement - maintenance or increase because an event/stimulus occurs as a consequence. (something plesant occurs)
  • Negative Reinforcement - maintenance or increase because an event/stimulus ceases or is prevented as a consequence (something unpleasant ceases)

e.g.,

NEG: client with bird phobia avoided or ran way from birds - these behaviours were negatively reinfoced by prevention (because there was less anxiety)

194
Q

According to operant conditioning, what types of consequences cease or reduce a behaviour?

A
  • Positive punishment - unplesant event/stimulus occurs as a consequence
  • Negative punishment - plesant even’t/stimulus is removed as a consequence

also. ..
* Extinction - reduction or cessation of behaviour because reinforcement is discontinued

195
Q

What are “discriminative stimuli”?

A

Stimuli that signal the likely reinforcement or non-reinforcement (or punishing consequence) of a behaviour

Signals to an organism that, should a particular response be made, reinforcement is available. Such a response is said to be under stimulus control because the response is usually made when only the discriminative stimulus is present.

Example: Alicia knows that her business partner is in a good mood if she is smiling, is not wearing her suit jacket, and has opened the blinds. These discriminative stimuli inform Alicia that she can approach her partner with a new idea (Alicia’s particular response) and expect her partner to be supportive (reinforcement). Alicia’s behavior is under stimulus control because Alicia will not approach her partner unless the discriminative stimuli are present.

196
Q

_________are stimuli that signal the likely reinforcement or non-reinforcement (or punishing consequence) of a behaviour

A

Discriminative stimuli

197
Q

What are the general treatment implications of Operant Conditioning theory?

A
  • Reinforce desirable behaviours
  • Reinforce behaviours incompatible with undesirable behaviours
  • Withdraw reinforcement for undesirable behaviour (Extinction)
  • Prevent punishment of desirable behaviour (Teach skills)
  • Stimulus control procedures (e.g., alco man avoids pub, then drives past, then walks past)
  • Shaping: reinforcing succssive approximations to the desire behaviour (e.g., for a client with bird phobia, for successfull steps taken in graded exposure)
198
Q

What is observational learning?

A

Learning behaviours by observing someone else (model) perform them.

Whether we perform observed behaviour depends on cosequences of the behaviour for the model.

  • positive consequences - increased chance
  • negative consequences - decreased chance
199
Q

What are the treatment implications of observational learning?

A
  • Model desired behaviour
    e. g., holding a bird to show a client with bird phobia that it is safe.
200
Q

Describe the general idea behind cognitve theories (Beck) in regard to abnormal psychology.

A

Cognitive theories emphasise people’s appraisal of events/stimuli, and underlying beliefs.

Thus, abnormal behaviour is thought to be caused by abnormal beliefs, intepretations and thoughts.

201
Q

What are “schema”?

A

An Underlying belief. Schemata affect attention, interpretation, memory.

In psychological disorders, schemata are abnormal negative.

202
Q

________ are ways of misintepreting info/event to fit schemata

A

Cognitive distortions

203
Q

________ are spontaneous thoughts about a given situation

A

Automatic thoughts

204
Q
  1. Recurrent and persistant thoughts, urges, or images that are… intrusive or unwanted, and in most individuals cause marked anxiety or distress
  2. The person attempts to ignore, supress or ‘neutralise’ them.

What does this describe?

A

Obsessions

205
Q

What is the relationship among the cognitive constructs (Schema, cognitive distortions and negative automatic thoughts)?

A

Schemata (Stable) -> cognitive distortions (biases in processing of a given situation) -> negative automatice thoughts (situation-dependant)

206
Q

Give an example (using a ‘bird phobia’) of the relationship between the cognitive constructs: schemata, cognitive distortions and negative automatice thoughts.

A
  • Schemata - birds are dangerous and unpredicatable, I can’t cope if I see a bird
  • Cognitive distortions - magnifiy and overgenearalise negative infor about birds; arbitary inference (inferring ngative things about birds with no evidence)
  • Negative Automatic Thoughts - “that bird will peck my eyes”, “it knows I am afraid”; “my hearts pounding, I’ll pass out”
207
Q

What are the treatment implications of cognitive theories?

A

AIM - identify & change negative automatic thoughts

  • Monitor & challenge negative automatic thoughts and dysfunctional beliefs
  • Substitute alternative adaptive thoughts
  • Often involves keeping a diary
208
Q

In OCD what are obsessions? (according to DSM-5 criteria)

A
  1. Recurrent and persistant thoughts, urges, or images that are… intrusive or unwanted, and in most individuals cause marked anxiety or distress
  2. The person attempts to ignore, supress or ‘neutralise’ them.

Themes include: dirt/contamination; death/injury; violence/sex.

Obsessions often occur in response to a recognised trigger.

209
Q

In OCD, what are compulsions? (According to DSM criteria)

A
  1. Repetitive behaviours (e.g., washing, ordering, checking)… or metal acts (e.g., praying, counting, repeating words) that the person feels driven to perform in response to an obsession.
  2. …aimed at preventing or reducing anxiety or distress, or preventing some dreaded event or situation” excessive and not relistically connected to their purpose.

Compulsions are intended to achieve one of the following

  • Avoidance (of triggers/obsessions)
  • Prevention
  • Putting things right; verification

*compulsions reduce anxiety*

210
Q
  1. Repetitive behaviours (e.g., washing, ordering, checking)… or metal acts (e.g., praying, counting, repeating words) that the person feels driven to perform
  2. …aimed at preventing or reducing anxiety or distress, or preventing some dreaded event or situation” excessive and not relistically connected to their purpose.

what does this describe?

A

Compulsions

211
Q

_____ is A compulsion to check repeatedly to ensure a task has been succesfully carried out or that a particular negative event has not occured.

A

checking

212
Q

______ is The compulsion to repeat a task/s in a particular way until it ‘feels right’.

A

repeating

213
Q

In OCD Counting

Repeating phrases e.g., “I hate the devil, I hate the devil”
Neutralising anxiety-provoking image by imagining the opposite

are all examples of what?

A

Mental acts

214
Q

In OCD, what is “hoarding” associated with?

A

Associated with a fear with losing information or objects, or a fear that objects can harm others (e.g., family or strangers)

215
Q

What is the “insight” specifier of OCD?

A

How much awareness one has of their OCD

Good or fair insight
poor insight
absent insight (Delusional)

216
Q

What are common comorbid conditions of OCD?

A

Deppression, anxiety disorders; tourette’s disorder (5-7%).

217
Q

(aetiology) How does learning theory explain OCD?

A

Based on Mowrer’s (1960) two-stage theory - combines classical conditioning and operant learning.

Classical conditioning: Neutral objects/situations/thoughts (e.g., locking door, passing though of car accident) become anxiety-provoking through being paired with an anxiety-provoking event (or anxious thoughts). Genaralisation to similar stimuli can occur.

Operant Learning (consequences): Avoidance (e.g., of triggers & obsession) is negatively reinforced by decreasing or prevention of anxiety but….

Many tiggers obsessions cannot be avoided, so…

Compulsions used to prevent harm or neutralise obsession, thus compulsions are negatively reinforced (Reduced anixety)

218
Q

(Aeitiology) how does cognitive theory explain OCD?

A
  • Individuals with OCD overestimate the probability & severity of threat.
  • Intrusive thoughts become obsessions when they are associated with negative automatic thoughts about responsibility. for causing (and preventing) harm.
  • Also importance of controlling thoughts; overestimation of importance of thoughts (e.g., that they increase risk)
  • Obsessions lead to perceptions of danger
  • Person feels they must act to avert/lessen danger, leading to compulsions.
219
Q
  1. (Aeitiology) how do biological models explain OCD?
  2. Do biological abnormalities associated with OCD indicate that they CAUSE OCD?
A

1.

  • Quite a few studies using PET scans and other neuroimaging techniques suggest abnormal activity in the nerve pathways connecting the basal ganglia and orbitofrontal cortex - these pathways use serotonin
  • There is a relationship between OCD & other disorders associated with abnormalities of the caudate nucleus
  1. NO

The biological abnormalities may or may not be causal. Behavioural changes have been shown to cause brain changes.

220
Q

What are the three main types of treatment for OCD?

A
  1. Exposure and Response Prevention (ERP) - behavioural therapy
  2. Cognitive Therapy
  3. Drug Therapy

The behavioral and cognitive therapy are often combined (CBT!)

221
Q

Describe the treatment (therapy) for OCD based on learning theory.

A

Exposure and Response Prevention (ERP)

Technique:

  1. Exposure to avoided situations & direct contact with feared stimuli
  2. Prevention of compulsions, including thoughts - graded! and individually tailored!!

Self-directed ERP needed; but therapist-guided initially better outcomes

  • Exposure = In-session practice; guided practice in real life setting, therapise MODELs behaviour
  • Homework (self-guided ERP) = agreed tasks (dailyl diary), home work adherance is a strong predictor of therapeutic outcomes.
222
Q

What is the GOLDEN RULE of exposure therapy?

A

Each episode of exposure must continue until anxiety diminishes, because if client leave before anxiety diminishes - the fear/avoidance etc will be negatively reinforced

i.e., it will be just another experience of anxiety regarding obsession/triggers.

223
Q

What is the rationale behind Exposure and Response Prevention (ERP) in the treatment of OCD?

A
  1. Ongoing exposure to feared stimulus without performing the compulsions (though anxiety intially increase) results in habituation (Reduced anxiety)
  2. Successively lower levels of anxiety break association between feared stimuli & anxiety (Extinction of conditioned response)

Non-performance of the compulsion also weakens the association between obsessions (thoughts & fears) & compulsions

224
Q

Describe how OCD is treated based on cognitive theory.

(what is cognitive therapy, what are the elements of the therapy, how does it help OCD?)

A

Cogitive Therapy

  • Aims to challenge negative automatic thoughts & change underlying beliefs (Schemata), challenge and replace dysfunctional beliefs about the probability of harm and personal responsability.
  • Cognitive restructuring - client taught to (1) Identify anxiety-provoking thoughts (2) Challenge them (3) Rehearse more constructive alternatives.

Cognitive therapy elements:

  • Evidence for & against obsession-related beliefs
  • Re-assign probabilities
  • In session & homeword - homework= correct dysfunctional thoughts and beliefs in daily diary
225
Q

What kind of drug is used to treat OCDs?

A

Usually antidepressant medications.

226
Q

Is ERP or CT (and CBT) more effective in the treatment of OCD?

A

There are few direct studies.

When studies are done-well, ERP can be as good as full CBT and better than CT alone (but possibly comparable)

ERP tends to have larger effects than CT alone, but not always.

227
Q

is CBT or drug therapy better for treating OCD?

A

Probably CBT, but a combination can be effective (Depending on baseline severity)

While the short-term effects of drugs can be as good as CBT, the long-term gain of drugs is poor and relapse is common when drugs are ceased.

Drugs also have side-effects and many people do not want to take drugs or drop-out

228
Q

Why is Agoraphobia considered a seperate disorder to Panic disorder (PD)?

How does this complicate current discussions?

A

Partly because agoraphobia can exist in the absence of panic attacks or PD

nearly all previous research (both aeiological & treatment) on agoraphobia has been done in the context of Panic Disorder

229
Q

What are the symptoms of a panic attack according the the DMS-5?

A

4 of the following symptoms

  • Palpatations, pounding&/or rapid heart rate
  • Sweating
  • Trembling or shaking
  • Sensation of shortness of breath
  • Feelings of choking
  • Chest pain/discomfort
  • Nausea/abdominal distress
  • Dizziness, faintness or unsteadiness
  • Chills or heat sensations
  • Paraesthesia (numbness of tingling)
  • Derelisation (unreality)
  • Fear of losing control or going mad
  • Fear of dying
230
Q

According to the DSM-5 what are the criteria for a diagnosis of Panic Disorder (PD)?

A
  1. at least one Panic attack. unexpected with no obvious cues/triggers. (usually more)
  2. at least one of the attacks has been followed by 1 month (+) of one or both of the following
  • Persistant concern about having additional panic attacks or their consequences (e.g., of a heart attack or “going crazy”, includes concern of life-threatening illness, cardiac problems, social, losing control [including bladder], insanity)
  • A significant maladpative change in behaviour related to attacks (e.g., avoids exercise or unfamiliar places - includes avoiding increasd heartrate & places where PA might be embaressing or help might not be available; repeatedly seeking medical help; work absenteeism or resign job.
231
Q

How must panic attacks differ from those of other anxiety disorders in order to be considered a diagnosis for Panic Disorder?

A
  • MUST be uncued (unexpected or ‘out of the blue’)
  • Central features (and the starting point for worry and behaviour change)
  • Probably more frequent
232
Q

According to the DSM-5 what is the diagnostic criteria of Agoraphobia?

A
  1. Marked fear/anxiety about 2(+) of the following situations
  • Using public transport
  • Open spaces (parking lots, market places)
  • Enclosed spaces (shops, cinemas)
  • Standing in a line or in a crowd
  • Being outside of the home alone
  1. The individual fears or avoids these situations because of thoughts that escape might be difficult or help might not be available in the event of having **panic-like symptoms or other incapacitating or embaressing symptoms **
  2. Agoraphobia are avoided, require the prescence of a companion, orr are endured with intense fear or anxiety.
  3. The fear/anxiety is excessive

Avoidance Agoraphobia

233
Q

What are the 3 suggested aetiology of PD (including with comorbid agoraphobia)?

A
  1. Hyperventilation
  2. Cognitive theory
  3. Learning - classical conditioning, operant conditioning
234
Q

How might hyperventilation explain Panic Disorder?

A

When we exhale, we excrete carbon disoxide (CO2) from our lung.

When people are frightened they hyperventilate - over-breath.

  1. Hyperventilation -> decrease CO2
  2. Decreased CO2 -> increased alkalinity
  3. increased alkalinity -> physical & psychological symptoms of panic
235
Q

How might cognitive theory explain Panic Disorder?

A
  • Individuals have an enduring disposition to intepret bodily sensation in a catastophic way (e.g., they will have a heart-attack, stroke, go mad or die)

Anxiety increased, bodily sensations increase; continues in vicious cycle -> panic attack

Increasing attentiveness to boily sensations and avoidance of place where panic could occur.

236
Q

What are the problems with cognitive theory as an explaination for Panic Disorder?

A
  1. Catastrophic cognitions about physical sensation can follow rather than precede the very first attack.
  2. Some people (30%) do not report fearing that bodily symptoms indicate impending mental or physical disaster
  3. Panic attacks can occur during non-dreaming sleep

i.e., not caused by the intepretation of bodily sensations in a catastrophic way.

237
Q

How do learning theories explain Panic Disorder?

A

Combined operant and classical conditioning

Classical:

  • Stressfull experience -> anxiety & first panic
  • Other internal & external stimuli present at the time become conditioned stimuli (CSs) that can lead to further attacks (CRs)

Operant:

  • Avoidance (e.g., of physical sensations associated with panic attacks [e.g., exercise]; general places that increase concern about having a PA; specific places where a PA occured before.
  • Avoidance is maintained by negative reinforcement (prevention/reduction of anxiety and panic attack themselves)
238
Q

How does cognitive theory and learning theory contrast in their explanations for the Panic Disorder?

(think, direction of relationship between beliefs, body sensations/panic, avoidance etc)

A

Cognitive theory i.e. beliefs -> avoidance

  • Dysfuntional beliefs about the meaning of bodily sensations -> panic attacks and avoidance

Learning theory i.e., body sensation/panic -> beliefs

  • Conditioned associations between bodily sensations (&situations) and panic –> beliefs/fears about bodily sensations. Avoidance neg. reinforced by reduced anxiety.
239
Q

What treatment for Panic Disorders is based on the hyperventilation theory?

A

Breathing retraining (to prevent/stop hyperventilation)

240
Q

What drug therapies are used to treat Panic DIsorder?

A
  • Antidepressant medications (a range of types)
  • Benzodiazepines (sedatives/sleeping pills) substantial risk of tolerance & dependence - not a good idea.
241
Q

What psychological therapies are used to treat Panic DIsorder?

A

Cognitive Behavioural Therapy (CBT)

242
Q

What is the most proven treatment for Panic DIsorder?

What does it involve?

A

Cognitive Behavioural Therapy

The most empirically supported psychosocial treatment for PD/A.

The central focus is repeated exposure to feared situations and sensations supported by a set of control-based coping skills.

“coping skills” = cognitive therapy plus breathing retraining and relaxation.

It involves:

  • Teaching client to identify catastropihic intepretations of boidly symptoms
  • Challenege; replace with rational response
  • Diary & daily homework exercises (often workbook)
243
Q

How is behaviour therapy used to treat Panic Disorder?

A

Exposure therapy to 1. sensations and 2. situations

Graded Interoceptive Exposure (to sensations)

244
Q

What is Graded Interoceptive Exposure used to treat and what is it?

A

Used to treat Panic Disorder (and Agoraphobia)

  • Graded exposure to physical sensations associated with panic attacks (CSs that trigger attacks)
  • Initially in presence of therapist; later, by the client at home.
  • Daily exercises

Purpose:

to breain associations b/t internal (interoceptive) sensations and panic reactions - extinction of CR

245
Q

How is behavioural therapy used to treat agoraphobia?

A

Graded exposure to feared situations/stimuli

  • Usually therapist-assisted initially, because therapist-guided has a better outcome for PD with agoraphobia.
  • Self-direct exposure also essential - daily homework
246
Q

is Cognitive therapy or Behaviour therapy (including hyperventilation) a better treatment for Panic Disorder (and agoraphobia)?

A

Recent meta-analyses indicated exposure (interoceptive & in-vivo) combined with breathing retraining has the largest therapeutic effects for PD (“Exposure is the treatment of choice”)

  • CT useful for panic attacks
  • Exposure therapy useful at managing avoidance
  • Introceptive exposures alone, improves beliefs about panic attacks.
  • Exposure for agoraphobia improves cognitions re. panic attacks & reduces frequency of panic attacks.
247
Q

IS psychological therapy or medication a better treatment for Panic Disorder?

A
  • Antidepressant medications and CBT either comparable, or CBT better.
  • Drop-outs tend to be lower for CBT than for drug therapy
  • More relapse with medication than CBT

They can be COMBINED, this sometimes results in better outcomes than either alone (e.g., quicker response), particularly for those with severe symptoms and comorbid deppression.

248
Q

What are the three types that symptoms of schizophrenia are commonly divided into?(As opposed to the orginal two)

A
  1. Positive - presence of abnormal behaviour
  2. Disorganised
  3. Negative - Deficit in normal behaviour
249
Q

Give some examples of Positive symptoms of schizophrenia.

A

Delusions, hallucinations etc

250
Q

Give some examples of disorganised schizophrenia symptoms.

A

Disorganised speech, grossly disorganised or catatonic behaviour

251
Q

Give some examples of negative schizophrenia symptoms.

A

Affective flattening, alogia, avoilation

252
Q

Outline the diagnostic criteria of schizophrenia

A

essentially - A. symptoms, B. Dysfunction, C. Duration

A Symptoms: two (+) of the following symptoms, each present for a significant portion of time in a 1-month period (or less if successfully treated. Must include 1, 2 or 3 .

  1. Delusions
  2. Hallucinations
  3. Disorganised speech (e.g., frequent derailment or incoherence)
  4. Grossly disorganised or catatonic behaviour
  5. Negative symotms (e.g., affective flattening, alogia, avoilition, anhedonia)

B Dysfunction - for a sig. portion of time since onset, lvl of functioning in one or more major areas, asuch as work, interpersonal relations or self-care, is markedly below the level achieved prior to onset.

C Duration - continuous signs of disturbance for 6+ months. at least 1 month of criterion A symptoms (unless successfully treated) may include preodromal (leading up to) or residual symptoms (after the acute phase)

253
Q

What symptoms MUST be present for a disgnosis of schizoprhenia?

A

Delusions, hallucinations or disorganised speech

254
Q

(in schizophrenia) What are delusions?

A

Delusions are bizzare false beliefs.

255
Q

________are the belief that someone/something is trying to harm them (e.g., spying following, posioning)

A

delusions of persection (i.e., paranoid delusions)

256
Q

The delusion of persecution whereby a person believes that someone or something is reading thoughts is known as ____

A

thought broadcast

257
Q

The delusion of persecution whereby a person believes that something is making them think things

A

thought insertion

258
Q

The delusion of persecution whereby a person believes that something is making them do things

A

made acts

259
Q

Belief the one has extraordinary powers (control the sun or wind) or that one is a very important person (e.g., God, bill gates, sent to prevent WW1)

A

Delusions of grandeur

260
Q

a type of delusion whereby a person sees personal significance/messages in events unrelated to them.

A

delusions of reference

261
Q
A
262
Q

(schizophrenia) what are hallucinations?

A

Flase perceptual experiences (mostly auditory 70%, mostly hearing voices)

263
Q

Activity occurs in what part of the brain when a person is experience auditory hallucinations?

A

Primary auditory cortex.

264
Q

What is disorganised speech (schizophrenia)?

A

Frequent dereailment or incoherence

265
Q

What is grossly disorganised or catatonic behaviour? (schizophrenia)

A

Movement abnormalities, profoundly dettached, stationary, catatonic posturing. In appropriate, purposless, unable to plan and execute tasks.)

examples include:

  • ties a ribbon around toe
  • points at nothing
  • standing in a corner
  • Inappropriate verbal behaviour and affect, e.g., mumbling, swearing, giggling.
266
Q

(negative symptoms - schizophrenia), what is Alogia?

A

Poverty of speech

267
Q

(negative symptoms - schizophrenia), what is avoilition?

A

Reduction in goal-directed behaviour.

268
Q

(negative symptoms - schizophrenia), what is anhedonia?

A

Reduction in the ability to experience pleasure.

269
Q

What is the prevalence, sex ratio and age of onset for schizophrenia?

A

Lifetime prevalence 1%

male:female = 1:1, BUT - sex differences in the natur of the disorder trajectory.

Age of onset = late to adolescent to early adulthood////

MEN - 15-24, drops of quickly

WOMEN - age of onset late for women

270
Q

Describe the course of schizophrenia. (ONSET, COURSE)

A

ONSET - can be gradual or acute (Sudden)

COURSE - highly variable

  • Frequency of relapse (Acute episodes)
  • Chronicity (persistance of symptoms)
  • Level of functioning between episodes
  • Symptoms
  • Cognitive functioning (Executive function, memory)

following acute episodes - 25-30% have chroni/persistant symptoms., 50%+ of schizophrenia is episodic (i.e., relapses), 45% have periods of recovary./remission (approximations based on a number of studies)

271
Q

What are the predictors of schizophrenia course/prognosis? which is the best?

A
  • Premorbid adjustment (is the BEST predictor) - people with good premorbid adjustment have a better prognosis.
  • Onset - gradual & earlier has a poorer prognosis.
  • Duration of untreated psychosis - longer -> worse
  • Symptoms - prominent negative symptoms lead to more chronic disorder, poorer social and work adjustment, less symptom relief from medication& cognitive impairment.
  • Sex - women tend to be better adjusted.
272
Q

large diversity in course, symptoms, treatment response, functioning and disability has led some researchers to re-term/rename schizophrenia to…?

A

Scizophrenias OR schizophrenic spectrum disorder

273
Q

Are people with schizophrenia more aggressive?

A

Overall, there probably is a higher rate of aggressive behaviour in people with schizophrenia than in
the general population, but “the vast majority are not aggressive” (DSM‐5, p. 101), & serious violence is rare.

274
Q

Activity occurs in what part of the brain when a person is experience auditory hallucinations?

A

Primary auditory cortex.

275
Q

What is disorganised speech (schizophrenia)?

A

Frequent dereailment or incoherence

276
Q

What is grossly disorganised or catatonic behaviour? (schizophrenia)

A

Movement abnormalities, profoundly dettached, stationary, catatonic posturing. In appropriate, purposless, unable to plan and execute tasks.)

examples include:

  • ties a ribbon around toe
  • points at nothing
  • standing in a corner
  • Inappropriate verbal behaviour and affect, e.g., mumbling, swearing, giggling.
277
Q

(negative symptoms - schizophrenia), what is Alogia?

A

Poverty of speech

278
Q

(negative symptoms - schizophrenia), what is avoilition?

A

Reduction in goal-directed behaviour.

279
Q

(negative symptoms - schizophrenia), what is anhedonia?

A

Reduction in the ability to experience pleasure.

280
Q

What is the prevalence, sex ratio and age of onset for schizophrenia?

A

Lifetime prevalence 1%

male:female = 1:1, BUT - sex differences in the natur of the disorder trajectory.

Age of onset = late to adolescent to early adulthood////

MEN - 15-24, drops of quickly

WOMEN - age of onset late for women

281
Q

Describe the course of schizophrenia. (ONSET, COURSE)

A

ONSET - can be gradual or acute (Sudden)

COURSE - highly variable

  • Frequency of relapse (Acute episodes)
  • Chronicity (persistance of symptoms)
  • Level of functioning between episodes
  • Symptoms
  • Cognitive functioning (Executive function, memory)

following acute episodes - 25-30% have chroni/persistant symptoms., 50%+ of schizophrenia is episodic (i.e., relapses), 45% have periods of recovary./remission (approximations based on a number of studies)

282
Q

What are the predictors of schizophrenia course/prognosis? which is the best?

A
  • Premorbid adjustment (is the BEST predictor) - people with good premorbid adjustment have a better prognosis.
  • Onset - gradual & earlier has a poorer prognosis.
  • Duration of untreated psychosis - longer -> worse
  • Symptoms - prominent negative symptoms lead to more chronic disorder, poorer social and work adjustment, less symptom relief from medication& cognitive impairment.
  • Sex - women tend to be better adjusted.
283
Q

large diversity in course, symptoms, treatment response, functioning and disability has led some researchers to re-term/rename schizophrenia to…?

A

Scizophrenias OR schizophrenic spectrum disorder

284
Q

Are people with schizophrenia more aggressive?

A

Overall, there probably is a higher rate of aggressive behaviour in people with schizophrenia than in
the general population, but “the vast majority are not aggressive” (DSM‐5, p. 101), & serious violence is rare.

285
Q

Is schizophrenia genetic? how do we know?

A

Part-genetic, part-environmental. Twin studies have shown a cocordance rate of 50% (approx) between monzygotic twins (i.e., identical twins).

Adoption studies have shown that BIOLOGY rather than rearing environment determines the risk of developing schizophrenia.

BUT the genetic picture is COMPLEX - spcific gene sunknown, multiple genes over multiple chromosomes are candidates, this might explain why it is so diverse.

286
Q

What structural abnormalities (brain) are present in some people with schizophrenia?

A
  • Ventricuular enlargement (atrophy), correlated with negative symptoms.
  • Reduced activity in frontal lobe, particularly during cognitive tasks - greatest with negative symptoms.
  • Neurotransmitter abnormalities - Dopamine hypotheses(more detail in another Q)
287
Q

What is the “dopamine hypothesis” for schizophrenia?

A

That schizophrenia reflects abnormalities of dopamine (DA)

  • Underactivity in frontal cortex (might) develop first and lead to overactivity in subcorticol areas!
  • underactivity in the frontal cortex -> negative symptoms
  • Overactivity in subcorticol parts -> positive symptoms.
288
Q

What three points of evidence are there for the “dopamine hypothesis” for schizophrenia?

A
  1. Antipsychotic drugs WORK because they reduce subcorticol dopamine activity.
  2. Antipsychotics side-effects - can produce symptoms of parkinson’s due to inadequote DA activity in the nigrostriatal pathway that deals with movement.
  3. Side effects of drugs that cause an increase in Dopamine e.g., ampetamines —> psychotic symptoms. ‘amphetamine psychosis’. OR L-dopa used to treat parkinsons disease can lead to psychosis.
289
Q

Overall, in schizophrenia _____ symptoms might reflect: reduced corticol activity (D1 receptors) & atrophy in the frontal lobes.

A

NEGATIVE

290
Q

Overall, in schizophrenia _____ symptoms might reflect: excessive dopamine activity (D2 receptors) in lower (subcorticol) parts of the brain).

A
291
Q

In schizophrenia frontal lobe ______ (____symptoms)may lead to subcorticol _______ (______ symptoms)

A

Underactivity (negative), Overactivity (positive)

292
Q

What is the Diathesis-stress hypothesis for schizophrenia?

A
  • Biological vulnerability + environmental stressor = schizophrenia.
  • Stressors include prenatal and birth complications, e.g., maternal infections and other illnesses, obstetric (e.g., oxygen deprivation, CNS trauma)
293
Q

the _________ for schizophrenia suggests that it is caused both by a combination of Biological vulnerability and environmental stressor/s

A

Diathesis-stress hypothesis

294
Q

What is the key intervention/treatment for schizophrenia?

A

Drug treatment, antipsychotics and neuroleptics.

295
Q

What % of ppl benefit little from drug treatment for schizophrenia?

A

10-30%

296
Q

How do antipsychotic medications work?

A
  • They decrease DOPAMIE activity in the lower parts of the breain by blocking post-synaptic DA receptors (attach/bind them without activation them and prevent DA from attaching to them)
297
Q

What is the non-adherance rate for medication int he treatment of schizophrenia?

A

50%+ over 12 months reduce dose or stop

298
Q

Why might people non-adhere to medication treatment for schizophrenia?

A
  • Remission
  • Perception thtat they don’t work (this can be correct)
  • Lack of insight
  • other drug problems, inadequote social support, homelessness
  • side effects of antipsychotic drugs.
299
Q

What are the extra-pyramidal side effects of ‘typical’ (i.e. first gen) antipsychotics?

A

Extra-pyramidal are movement symptoms and relate to the drugs effect on the nigrostriatal pathway (dopamine pathway).

e.g.,

  • Akathisia = restelessness
  • Actue dystonic reactions - sudden, painful muscle spasms
  • Drug-induced parkinsons
  • Tardive dyskinesia - mouth and tongue movements.
300
Q

What is the name given to extrapyramidal side-effect of 1st gen (‘typical’) antipsychotic drugs involving restlessness

A

Akathisia

301
Q

What is the name given to extrapyramidal side-effect of 1st gen (‘typical’) antipsychotic drugs involving sudden, painful muscle spasms?

A

Acute Dystonic reactions

302
Q

What is the name given to extrapyramidal side-effect of 1st gen (‘typical’) antipsychotic drugs involving mouth and tongue movements

A

Tardive dyskinesia

303
Q

What are some of the side effects of ‘typical’ (first gen) antipsychotics?

A

dizziness, dry mouth, constipation, trouble urination, sedation, anxiety and depression + extra-pyramidal.

304
Q

____________ side-effects are movement related results of taking ‘typical’ nueroleptic/antipsychotic drugs.

A

Extra-Pyramidal

305
Q

What are the benefits of 2nd generation (‘atypical’) antipsychotic drugs over 1st generation (‘typical’) ?

A
  • Greater potential to reduce negative symptoms (& disorganised symptoms)
  • Extra-pyramidal (movement) side-effects are less common and less sever (but may still occur).
306
Q

How to 2nd gen antipsychotics work different to 1st gen?

A
  • They both block dopamine receptors, but 2nd gen to a lesser extent
  • 2nd gen also block certain serotonin receptos (5-HT, 2A) to help prevent extrapyramidal side-effects by preserving the DA function in nigrostriatal pathway.
307
Q

What are the side effects of 2nd generation antipsychotics?

A
  • sedation, sleepiness, dry mouth, insomnia, dizziness, headaches, sexual problems, increase blood cholesterol, weight gain, diabetus.
308
Q

What role does psychological treatment (i.e. CBT) have in treating schizophrenia?

A
  • Promote management of symptoms
  • Reduce relapse
  • Promote self-care skills and social & occupational skills where relevant
  • coping with symptoms such as delusions and hallucinations
  • treat comorbid conditions such as depression or drug dependance.
309
Q

_______ in scizophrenia includes: Movement abnormalities, profoundly dettached, stationary, catatonic posturing. In appropriate, purposless, unable to plan and execute tasks.)

A

Grossly disorganised or catatonic behaviour

310
Q

_____ is Poverty of speech

A

Alogia

311
Q

_____ is a reduction in goal-directed behaviour

A

Avoilition

312
Q

____ is a reduction in the ability to experience pleasure.

A

Anhedonia

313
Q
A
314
Q

What components of CBT focuses on negative symptoms, what part focuses on positive symptoms?

A

Negative - activity scheduling

Positive - teaching people to ….

  • consider possibilitthat hallucinations come from within their own minds
  • evaluate the plausibility of delusions by considering evidence & alternative explanations
  • Using behavioural experiments.
315
Q

What is the diagnostic criteria for Major depressive disorder (DSM5)?

A

A. MAJOR DEPRESSIVE EPISODE five of the following symptoms must be present for at least 2 weeks. Must include 1 or 2.

  1. depressed mood (sad, empty, hopeless, tearful)
  2. loss of interest/pleasure in usual activities
  3. Poor appetite & weight loss, or increased appetite and weight gain
  4. Sleeping difficulties
  5. Psychomoto agitation or retardation
  6. fatigue
  7. feelings of worthlessness or excessive inappropriate guilt
  8. reduced concentration or ability to think
  9. recurrent thoughts of death or suicide plans/attempts.

B. Symptoms -> clin sig. distress or impairment in social occupational or other important area of functioning.

C. never been a manic or hypermanic episode

316
Q

What is the DSM-5 criteria for Bipolar 1 disorder?

A

A. Manic episode - distinct period of abnormal & persistantly elevated expansive, or irritable mood and persistently increased goal-directed activity or energy lasting at least 1 week and present most of the day, every day (or any duraction if hospitalisation is required)

+

B. At least 3 of the following (or 4 if only irritated not elevated mood)

  • inflated self-esteem or grandiosity (includes grandiose dellusions)
  • decreased need for sleep
  • more talkative than usual or pressure to keep talking
  • flight of ideas or subjective impression thoughts are racing
  • distractability; attention easily diverted
  • increase in goal-directed activity
  • excessive involvement in pleasurable activities that have high potential for painfull consequences

C. the mood disturband is sufficiently severe to cause marked IMPAIRMENT (note: no distress criteria)

317
Q

what % of people suffering bipolar have delusions (i.e., psychotic features)?

A

approx 40%

318
Q

how does the psychosocial & occupational functioning of people with bipolar compare to those with schizophrenia?

A
  • Bipolar better than schizophrenia
  • full functioning recovary between episodes more likely in bipolar
  • BUT substatial proportion of those with bipolar still experience sig. ongoing problems (residual symptoms, impaired functioning)
319
Q

What factors predict poor outcomes for people suffering with bipolar1 ?

A

Depressed or mixed symptoms in 1st episode( rather than pure mania)

earlier onset

comorbid drug dependence

320
Q

after the 1st manic episode (in bipolar1), what % have a future episode and how many relapse (to depression or mania) in a 2-year period?

A

90%

50% (1/2)

321
Q

What is the prevalence of major depressive disorder (lifetime)

A

up to 16% experience severe incapacitating depression

322
Q

Prevalence of bipolar 1 disorder? (lifetime)

A

0.6%

323
Q

is the suicide rate higher in bipolar or major depressive disorder?

A

Enourmasly elevated in bipolar 1 disorder, but still elevated in major depression.

324
Q

What is the twin concordance rate vs. fraternal rate for Major depressive disorder? what does this suggest?

A

identical twins 40%, fraternal twins 20% - (rubbery evidence though!)

A probably genetic component.

325
Q

What is the twin concordance rate vs. fraternal rate for bipolar1? what does this suggest?

A

identical twins 50-60%, fraternal twins 20%

A probably genetic component.

326
Q

How is it theorised that bipolar1 affects neurotransmitters?

A

Neurotransmitters – Dopamine, noradrenaline (norepinephrine) ELEVATED; serotonin deficient.

327
Q

How is it theorised that major depressive disorder affects neurotransmitters?

A

– Serotonin, noradrenaline and dopamine deficient.

328
Q

outline the behavioural/learning theory model fo major depressive disorder.

A

Behaviour/learning theory –
Extinction of desirable behaviours (inadequate reinforcement for desirable behaviour – lack of skill or poor environment).

non-reinforced behaviours are extinguished - person becomes withdrawn, avoidant and inactive - negative affect

Reinforce depressed behaviour – sympathy/enabling.

329
Q

What is Beck’s cognitive theory of major depressive disorder?

A

Cognitive theory –Beck’s negative self-schema model – depression due to negative thinking. Cognitive biases.

  • Person vulnerable to depression owing to cognitive schemata in whcih the self, world and future are seen as negative (from negative childhood events) (these schemata are stable).
  • Stressfull events can activate the schemata
  • Cogntive distortions/biases = life events interpreted in a way consistant with schemata (e.g., exaggerate failures, minimise successes) - strengthen schemata
  • Negative automatic thoughts reflect congitive distortions in a given situation.
330
Q

in Major depressive disorder (and bipolar 1) what is the relationship between biology and behaviour/mood?

A

Neurotransmitter abnormalities affect behaviour & mood

Behaviour and mood affect neurotransmitter activity

e.g., chronic environmental stress reduces noradrenaline

physical activity affects neurotransmitters

Behaviour/mood neurotransmitter activity

331
Q

Give some examples of types of cognitive distortions (seen in major depressive disorder according to Beck’s negative self-schema model)

A
  • Personalisation (attributing personal responsability)
  • selective abstraction (focusing on only neg aspects of an event)
  • Magnification & minimisation (magnify negative, minimise positive)
  • Arbitary inference (mind-reading)
  • Expecting the worse
  • over-generalisation
  • all or nothing thinking
  • catastrophising
332
Q

How to antidepressants work to treat major depressive disorder? and bipolar1?

A

MDD: depressed mood associated with reduced serotonin and noradrenalin. antidepressant medicine aims to increase these.

bipolar 1: associated with increase noradrenaline and dopamine so drug treatments aim to optimise serotonin and stabalise Dopamine and noradrenaline (and other excitory neurotransmitters)

333
Q

How long does antidepressant medication usually take to take effect?

A

2-3 weeks up to 6 weeks for full therapeutic effect.

334
Q

What are the four types of antidepressant medications?

A

Monoamine oxidase inhibitors (MAOI)

Tricyclic acid (e.g., amitriptyline, imipramine)

Selective serotonin reuptake inhibitor (SSRIs) (e.g., fluoxetine, sertraline, paroxetine, fluvoxamine, citralopram)

Serotonin & noradrenaline reuptake inhibitors (SNRIs) (e.g., bupropion, venlafaxine)

335
Q

Why are MAOI antidepressants prescribed less frequently?

A

requires heavy dietary restrictions.

336
Q

How to Selective serotonin reuptake inhibitors work?

A

They block the reuptake of serotonin the neuron synapse, such that more serotonin stays in the synapse and is more availiable for tramission along the pathway.

337
Q

What is the “first line” of treatment for bipolar?

A

DRUGS!

Mood stabalisers e.g., lithium (effective dose is close to toxic dose) or valproate.

Anti-psychotics for acute mania

anti-depressants.

338
Q

adherance to medication in bipolar reduced the chance of relapse, but adherance in a problem with up to ___% non-adhering within 12 months of commencing treatment.

A

40%

339
Q

Why might people not adhere to drug treatments for bipolar1?

A
  • Remission
  • side-effects and fear of them
  • perceived ineffectiveness
  • comorbid drug-dependance
  • homelessness, low social support
  • they ENJOY the highs of mania
340
Q

How does cognitive-behavioural therapy supplement the drug treatment for bipolar 1?

A
  • promotes adherance to meds
  • helps recognise signs of relapse
  • protection during manic episodes
  • activity monitoring
  • sleep and stress maintenance (reduces relapse)
  • social/interpersonal problems)
  • others concerns (mood swings, maintaining jobs)
  • comorbid problems such as drug dependance.
341
Q

outline cognitive therapy as a treatment of Major depressive disorder.

A
  • AIM: teach clients to identify and challenge/refute irrational cognitions.
  • clients ask themself questions regarding the evidence, alternative intepretations and logical errors of their beliefs/cognitions.

reinterpretation and thought diary.

342
Q

As part of cognitive therapy for major depressive disorder what are “behavioural experiments”?

A

testing a prediction that a bad thing will happen when X happens.

  1. make a prediction “if i disagree with her she won’t like me”
  2. what evidence is there for and against the predicition
  3. plan specific way of testing the prediction
  4. test it. If necessary, learn positve new ways of engaging in the behaviour
  5. note the results and draw conclusions.
343
Q

What is the best treatment for major depressive disorder?

A

Best?

  • CT = BT
  • BT = CBT
  • CBT(60=70%) > drug (40-60%),

high placebo-drug effect (30%). Medication does not require skill & might make CBT easier, but drugs have a high dropout rate.

344
Q

What is the DSM-5 criteria for Dissociative Identity Disorder?

A
  • DSM-5 more GENERAL,

A. disruption of identity characterized by two or more distinct personality states (like possessions), alterations in affect, consciousness, memory, perception, cognition and/or sensory functioning.

B. gaps in recall of everyday events/important personal info

C. clinically significant distress or impairment.

D. disturbance not part of culture/religion.

345
Q

How did the DSM-4 and DSM-5 criteria for dissociative identity disorder differ?

A
  • DSM-4 required two or more distinct identities or personality states, that take over behaviour.
  • DSM-5 more GENERAL, just a disruption of identity.
346
Q

What is a factitious disorder?

A

deliberate production of symptoms to gain proffesional attention.

347
Q

What are some ALTERNATIVE models to the trauma model of dissociative identity disorder?

A
  • Diagnostic bias (incorrect or overdiagnosis)
  • suggestion and shaping during therapy - including hypnotic suggestion
  • publicity
  • simulation