PRACTICE EXAM + SUMMARY
ADVANCED CLINICAL
NEUROPSYCHOLOGY
PRACTICE QUESTIONS LECTURES WEEK 1 – WEEK 7
WEEK 1 - BRAIN DAMAGE AND FAMILY AFAIR
1. What is clinical neuropsychology and how does it combine psychology and
neurology to assess, diagnose, and treat cognitive, emotional, and behavioral
disorders resulting from brain damage?
2. Which three types of costs – direct healthcare costs, direct non-medical costs, and
indirect costs – are distinguished in cases of brain damage?
3. What is the purpose of neuropsychological assessments in identifying cognitive,
emotional, and behavioral disorders, and how do they justify the costs through
savings and an improvement in quality of life?
4. Why is the identification of malingering important, and how does it help to avoid
unnecessary treatments and extra medical costs?
5. How does an accurate diagnosis (for example, distinguishing between depression and
dementia) contribute to preventing ineffective treatments and saving costs?
6. In what way can a neuropsychological evaluation contribute to improving the quality
of life by addressing issues in executive functions and memory?
7. Why is evaluating the effectiveness of a treatment essential for making better
therapeutic decisions?
8. How can the results of a neuropsychological evaluation help determine the most
suitable rehabilitation strategy?
9. How does an early and accurate diagnosis prevent the use of more expensive
diagnostics?
10. What does the complete care trajectory include, and how does insight into diagnosis,
treatment, and aftercare contribute to the continuum of care?
11. What are the main transdiagnostic problems that people with neurological conditions
might experience as described in the lecture?
12. What does the profession of the clinical neuropsychologist involve according to the
lecture?
13. How is cost-effectiveness justified in clinical neuropsychological assessments based
on the lecture content?
14. Which key components are assessed during a clinical neuropsychological examination
for cost-effectiveness?
15. What financial figures illustrate the cost and revenue challenges of maintaining a
clinical neuropsychology department in the US?
16. How do medicolegal cases and research grants contribute to the revenue in clinical
neuropsychology?
17. What does the phrase "brain damage as a family affair" refer to in the lecture?
, 18. Which factors influence the severity of problems experienced by family members of
individuals with brain damage?
19. Which behaviors in individuals with brain damage are likely to create social problems
as mentioned in the lecture?
20. How do neuropsychological interventions help alleviate the burden on families
affected by brain damage?
WEEK 2 - FATIGUE
21. Define fatigue and discuss how it encompasses both a subjective lack of energy and
an objective performance decrement.
22. Explain the difference between pathological fatigue and non-pathological fatigue,
including the aspects of intensity, duration, and impact on daily activities.
23. Differentiate between primary fatigue and secondary fatigue. How do neural
mechanisms and external factors contribute to each?
24. Identify the main neurobiological correlates of fatigue mentioned in the lecture.
25. Discuss the advantages and limitations of using self-report questionnaires for
assessing fatigue.
26. Describe the challenges in correlating subjective fatigue with objective performance
measures.
27. What recommendations are provided to minimize the detrimental effects of fatigue on
neuropsychological performance during assessments?
28. Outline the main treatment strategies for fatigue, mentioning the roles of
psychotherapy, pharmacotherapy, and physical exercise.
29. How does physical exercise influence fatigue, and what evidence supports its use in
clinical populations such as people with multiple sclerosis?
30. Why is it important to consider both physiological and psychological factors when
managing fatigue, given its multidimensional nature?
WEEK 3 - DISORDERS OF AWARENESS
Practice questions week 3
31. What is the difference between anosognosia, impaired self-awareness, and denial, and
why is this distinction clinically important?
32. How can we distinguish denial of disability (DD) from impaired self-awareness (ISA)
during clinical assessment?
33. Why is anosognosia considered multifactorial, and what role might different brain
regions and neuropsychological functions play in its development?
34. What evidence suggests that some individuals with anosognosia still possess implicit
knowledge of their deficits?
35. How can the presence of anosognosia or ISA negatively influence rehabilitation
outcomes, and what are examples of these effects in stroke and traumatic brain injury?
36. Why is there no single, universally accepted method for assessing anosognosia, and
what are the advantages and disadvantages of caregiver ratings, clinical judgment, and
performance-based measures?
37. How do prediction and postdiction discrepancy methods work in measuring
awareness, and what makes Rosen’s (2011) approach unique?
38. What are some associated phenomena that can resemble or accompany anosognosia,
such as confabulation or alexithymia, and how do they differ from unawareness itself?
, 39. Which ethical issues arise when a person with significant ISA or anosognosia refuses
necessary treatment or continues unsafe activities (such as driving), and what role
should clinicians and surrogate decision-makers play?
40. What are possible strategies for managing ISA and denial in rehabilitation, and why is
proper management crucial for avoiding negative psychiatric and functional
outcomes?
WEEK 4 - SUICIDALITY IN PEOPLE WITH NEUROLOGICAL DISORDERS
41. What does the interpersonal theory of suicide propose regarding the role of thwarted
belongingness and perceived burdensomeness in suicidal behavior?
42. Why is it difficult to establish a specific time period of elevated suicide risk following
traumatic brain injury (TBI), and what does current evidence suggest about the
duration of this risk?
43. Which factors may explain the increased prevalence of depression in people with TBI,
and why is hopelessness considered a robust predictor of suicide?
44. How do pre-injury traits (such as substance abuse or aggressiveness) and post-injury
neurological changes each contribute to heightened suicidality in TBI?
45. Why might typical gender-related patterns of suicidality in the general population
(e.g., men dying by suicide more frequently) not apply to individuals with TBI?
46. What is meant by serotonergic hypofunction in the basal orbital region of the
prefrontal cortex, and how might it relate to impulsivity and aggression in the context
of TBI?
47. Which warning signs indicate a need for immediate intervention, and how do these
differ from warning signs suggesting the need for mental health treatment that may not
be urgent?
48. What are key components of a comprehensive clinical assessment for suicidality in
people with TBI, and why is it important to gather information from multiple sources?
49. How might rehabilitation and psychosocial interventions reduce suicide risk in
individuals with TBI, and why is social support a critical factor?
50. What considerations should be taken into account for emergency interventions (e.g.,
hospitalization) when a person with TBI expresses imminent suicidal intent?
WEEK 5 - SEXUAL FUNCTIONING IN PEOPLE WITH NEUROLOGICAL
DISORDERS
51. How can a brain injury directly and indirectly affect important aspects of sexual desire
and response?
52. Why might cognitive deficits such as distractibility, attention problems, and memory
impairments reduce sexual satisfaction in individuals with traumatic brain injury?
53. What roles do psychological and social factors (such as body image, depression, and
relationship changes) play in the sexual dysfunction observed in people with
neurological disorders?
54. How can temporal lobe epilepsy manifest in both ictal and interictal sexual behaviors,
and what role does the right hemisphere appear to play?
55. In what ways can the primary, secondary, and tertiary classifications of sexual
dysfunction in multiple sclerosis each influence a person’s sexual health?
56. Why is addressing sexuality important for optimal rehabilitation outcomes, and what
are potential barriers that prevent healthcare professionals from discussing sexual
issues?
, 57. Which neurological or medication-related factors can lead to hypersexuality, and how
does this differ from disinhibited sexual behavior?
58. What are some common reasons for a decline in sexual function after stroke, and how
might medication regimens contribute to this decline?
59. Why are interviews considered the most relevant assessment tool for evaluating sexual
functioning in neurological populations, and how can questionnaires complement
these interviews?
60. What is inappropriate sexual behavior (ISB) in the context of neurological disorders,
and why is distinguishing between hypersexuality and disinhibition important for
treatment?
WEEK 6 - ETHICS IN CLINICAL NEUROPSYCHOLOGY AND THE
CAPABILITY TO MAKE DECISIONS
61. What do the four principles of medical ethics (autonomy, justice, non-maleficence,
beneficence) entail, and why can relying solely on paternalism or isolated autonomy
be problematic?
62. Why is shared decision-making considered a more desirable approach in clinical
practice, and what potential barriers might hinder its implementation?
63. What are the four abilities that define a person’s capability to make medical decisions,
and why are standard neuropsychological tests often insufficient to assess these
abilities?
64. Why can wrong decisions about a person’s decision-making capacity lead to either
“wrongful loss of autonomy” or “wrongful maintenance of autonomy,” and why is this
ethically significant?
65. How do standardized vignettes differ from condition-specific vignettes in assessing
medical decision-making capacity, and what are the trade-offs between these two
approaches?
66. What are the five abilities used to assess a person’s capability to make financial
decisions, and why do contextual factors (e.g., social support, impulsivity) also
matter?
67. In the case examples of KS and JT, why was there a discrepancy between “knowing”
(i.e., good test performance or verbal explanation) and “doing” (i.e., actual
performance in everyday tasks), and how does this illustrate the complexity of
assessing capacity?
68. Why is capacity considered decision-specific, and how might a person be capable of
making some decisions (e.g., simple, low-risk) but not others (e.g., complex, high-
risk)?
69. What are the key principles from the NSW Government Capacity Toolkit regarding
capacity assessment, and why is it important to focus on a person’s decision-making
ability rather than the perceived quality of their decisions?
70. How might fluctuating or changing abilities (e.g., recovery from stroke or cognitive
fluctuations in dementia) complicate the assessment of a person’s capacity to make
decisions over time?
ADVANCED CLINICAL
NEUROPSYCHOLOGY
PRACTICE QUESTIONS LECTURES WEEK 1 – WEEK 7
WEEK 1 - BRAIN DAMAGE AND FAMILY AFAIR
1. What is clinical neuropsychology and how does it combine psychology and
neurology to assess, diagnose, and treat cognitive, emotional, and behavioral
disorders resulting from brain damage?
2. Which three types of costs – direct healthcare costs, direct non-medical costs, and
indirect costs – are distinguished in cases of brain damage?
3. What is the purpose of neuropsychological assessments in identifying cognitive,
emotional, and behavioral disorders, and how do they justify the costs through
savings and an improvement in quality of life?
4. Why is the identification of malingering important, and how does it help to avoid
unnecessary treatments and extra medical costs?
5. How does an accurate diagnosis (for example, distinguishing between depression and
dementia) contribute to preventing ineffective treatments and saving costs?
6. In what way can a neuropsychological evaluation contribute to improving the quality
of life by addressing issues in executive functions and memory?
7. Why is evaluating the effectiveness of a treatment essential for making better
therapeutic decisions?
8. How can the results of a neuropsychological evaluation help determine the most
suitable rehabilitation strategy?
9. How does an early and accurate diagnosis prevent the use of more expensive
diagnostics?
10. What does the complete care trajectory include, and how does insight into diagnosis,
treatment, and aftercare contribute to the continuum of care?
11. What are the main transdiagnostic problems that people with neurological conditions
might experience as described in the lecture?
12. What does the profession of the clinical neuropsychologist involve according to the
lecture?
13. How is cost-effectiveness justified in clinical neuropsychological assessments based
on the lecture content?
14. Which key components are assessed during a clinical neuropsychological examination
for cost-effectiveness?
15. What financial figures illustrate the cost and revenue challenges of maintaining a
clinical neuropsychology department in the US?
16. How do medicolegal cases and research grants contribute to the revenue in clinical
neuropsychology?
17. What does the phrase "brain damage as a family affair" refer to in the lecture?
, 18. Which factors influence the severity of problems experienced by family members of
individuals with brain damage?
19. Which behaviors in individuals with brain damage are likely to create social problems
as mentioned in the lecture?
20. How do neuropsychological interventions help alleviate the burden on families
affected by brain damage?
WEEK 2 - FATIGUE
21. Define fatigue and discuss how it encompasses both a subjective lack of energy and
an objective performance decrement.
22. Explain the difference between pathological fatigue and non-pathological fatigue,
including the aspects of intensity, duration, and impact on daily activities.
23. Differentiate between primary fatigue and secondary fatigue. How do neural
mechanisms and external factors contribute to each?
24. Identify the main neurobiological correlates of fatigue mentioned in the lecture.
25. Discuss the advantages and limitations of using self-report questionnaires for
assessing fatigue.
26. Describe the challenges in correlating subjective fatigue with objective performance
measures.
27. What recommendations are provided to minimize the detrimental effects of fatigue on
neuropsychological performance during assessments?
28. Outline the main treatment strategies for fatigue, mentioning the roles of
psychotherapy, pharmacotherapy, and physical exercise.
29. How does physical exercise influence fatigue, and what evidence supports its use in
clinical populations such as people with multiple sclerosis?
30. Why is it important to consider both physiological and psychological factors when
managing fatigue, given its multidimensional nature?
WEEK 3 - DISORDERS OF AWARENESS
Practice questions week 3
31. What is the difference between anosognosia, impaired self-awareness, and denial, and
why is this distinction clinically important?
32. How can we distinguish denial of disability (DD) from impaired self-awareness (ISA)
during clinical assessment?
33. Why is anosognosia considered multifactorial, and what role might different brain
regions and neuropsychological functions play in its development?
34. What evidence suggests that some individuals with anosognosia still possess implicit
knowledge of their deficits?
35. How can the presence of anosognosia or ISA negatively influence rehabilitation
outcomes, and what are examples of these effects in stroke and traumatic brain injury?
36. Why is there no single, universally accepted method for assessing anosognosia, and
what are the advantages and disadvantages of caregiver ratings, clinical judgment, and
performance-based measures?
37. How do prediction and postdiction discrepancy methods work in measuring
awareness, and what makes Rosen’s (2011) approach unique?
38. What are some associated phenomena that can resemble or accompany anosognosia,
such as confabulation or alexithymia, and how do they differ from unawareness itself?
, 39. Which ethical issues arise when a person with significant ISA or anosognosia refuses
necessary treatment or continues unsafe activities (such as driving), and what role
should clinicians and surrogate decision-makers play?
40. What are possible strategies for managing ISA and denial in rehabilitation, and why is
proper management crucial for avoiding negative psychiatric and functional
outcomes?
WEEK 4 - SUICIDALITY IN PEOPLE WITH NEUROLOGICAL DISORDERS
41. What does the interpersonal theory of suicide propose regarding the role of thwarted
belongingness and perceived burdensomeness in suicidal behavior?
42. Why is it difficult to establish a specific time period of elevated suicide risk following
traumatic brain injury (TBI), and what does current evidence suggest about the
duration of this risk?
43. Which factors may explain the increased prevalence of depression in people with TBI,
and why is hopelessness considered a robust predictor of suicide?
44. How do pre-injury traits (such as substance abuse or aggressiveness) and post-injury
neurological changes each contribute to heightened suicidality in TBI?
45. Why might typical gender-related patterns of suicidality in the general population
(e.g., men dying by suicide more frequently) not apply to individuals with TBI?
46. What is meant by serotonergic hypofunction in the basal orbital region of the
prefrontal cortex, and how might it relate to impulsivity and aggression in the context
of TBI?
47. Which warning signs indicate a need for immediate intervention, and how do these
differ from warning signs suggesting the need for mental health treatment that may not
be urgent?
48. What are key components of a comprehensive clinical assessment for suicidality in
people with TBI, and why is it important to gather information from multiple sources?
49. How might rehabilitation and psychosocial interventions reduce suicide risk in
individuals with TBI, and why is social support a critical factor?
50. What considerations should be taken into account for emergency interventions (e.g.,
hospitalization) when a person with TBI expresses imminent suicidal intent?
WEEK 5 - SEXUAL FUNCTIONING IN PEOPLE WITH NEUROLOGICAL
DISORDERS
51. How can a brain injury directly and indirectly affect important aspects of sexual desire
and response?
52. Why might cognitive deficits such as distractibility, attention problems, and memory
impairments reduce sexual satisfaction in individuals with traumatic brain injury?
53. What roles do psychological and social factors (such as body image, depression, and
relationship changes) play in the sexual dysfunction observed in people with
neurological disorders?
54. How can temporal lobe epilepsy manifest in both ictal and interictal sexual behaviors,
and what role does the right hemisphere appear to play?
55. In what ways can the primary, secondary, and tertiary classifications of sexual
dysfunction in multiple sclerosis each influence a person’s sexual health?
56. Why is addressing sexuality important for optimal rehabilitation outcomes, and what
are potential barriers that prevent healthcare professionals from discussing sexual
issues?
, 57. Which neurological or medication-related factors can lead to hypersexuality, and how
does this differ from disinhibited sexual behavior?
58. What are some common reasons for a decline in sexual function after stroke, and how
might medication regimens contribute to this decline?
59. Why are interviews considered the most relevant assessment tool for evaluating sexual
functioning in neurological populations, and how can questionnaires complement
these interviews?
60. What is inappropriate sexual behavior (ISB) in the context of neurological disorders,
and why is distinguishing between hypersexuality and disinhibition important for
treatment?
WEEK 6 - ETHICS IN CLINICAL NEUROPSYCHOLOGY AND THE
CAPABILITY TO MAKE DECISIONS
61. What do the four principles of medical ethics (autonomy, justice, non-maleficence,
beneficence) entail, and why can relying solely on paternalism or isolated autonomy
be problematic?
62. Why is shared decision-making considered a more desirable approach in clinical
practice, and what potential barriers might hinder its implementation?
63. What are the four abilities that define a person’s capability to make medical decisions,
and why are standard neuropsychological tests often insufficient to assess these
abilities?
64. Why can wrong decisions about a person’s decision-making capacity lead to either
“wrongful loss of autonomy” or “wrongful maintenance of autonomy,” and why is this
ethically significant?
65. How do standardized vignettes differ from condition-specific vignettes in assessing
medical decision-making capacity, and what are the trade-offs between these two
approaches?
66. What are the five abilities used to assess a person’s capability to make financial
decisions, and why do contextual factors (e.g., social support, impulsivity) also
matter?
67. In the case examples of KS and JT, why was there a discrepancy between “knowing”
(i.e., good test performance or verbal explanation) and “doing” (i.e., actual
performance in everyday tasks), and how does this illustrate the complexity of
assessing capacity?
68. Why is capacity considered decision-specific, and how might a person be capable of
making some decisions (e.g., simple, low-risk) but not others (e.g., complex, high-
risk)?
69. What are the key principles from the NSW Government Capacity Toolkit regarding
capacity assessment, and why is it important to focus on a person’s decision-making
ability rather than the perceived quality of their decisions?
70. How might fluctuating or changing abilities (e.g., recovery from stroke or cognitive
fluctuations in dementia) complicate the assessment of a person’s capacity to make
decisions over time?
