Clinical Neuropsychology. Introduction. Dr Alan Sunderland

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1 Clinical Neuropsychology. Introduction Dr Alan Sunderland 1

2 Overview What is a clinical neuropsychologist? Who are their clients? Principles of assessment. Assessment of memory problems Processes of recovery and rehabilitation. Rehabilitation for memory problems. Executive function and personality change Assessment of executive function Rehabilitation for executive dysfunction. 2

3 Reading List Kolb, B. & Whishaw I.Q. Fundamentals of human neuropsychology. Fifth Edition. Worth Publishers Chapters 18, 25 & 28. Goldstein L.H. & McNeil, J.E. Clinical neuropsychology : a practical guide to assessment and management for clinicians. John Wiley Especially, Chapter 9. Wilson, Barbara A. Case studies in neuropsychological rehabilitation. Oxford University Press

4 What is clinical neuropsychology? Its relationship to other aspects of Clinical Psychology An area of clinical psychology which uses evidence-based methods for the assessment, counselling and rehabilitation of the person with acquired brain damage. Most clinical psychologists work in general adult mental health, but there is a continual demand for specialist posts in areas such as neuropsychology. Many of the same skills are used (e.g. intervention for anxiety or depression) but the clinical neuropsychologist also requires knowledge of effects of brain damage. Assessment and treatment of cognitive impairment and personality change are unique to clinical neuropsychology and are fascinating and rewarding areas of work. 4

5 What is clinical neuropsychology? An example from Carpenter & Tyerman (1999) from What is clinical psychology Marzillier & Hall, Oxford Univ Press,1999 5

6 What is clinical neuropsychology? Its relationship to academic neuropsychology Clinical Neuropsychology An area of clinical psychology which uses evidence-based methods for the assessment, counselling and rehabilitation of the person with acquired brain damage. Academic Neuropsychology An area of cognitive neuroscience which studies effects of human brain damage to inform theories of normal cognitive processing. This has been the driving force behind most neuropsychological research, and clinical concerns can be neglected e.g. Kolb & Whishaw have only 1 chapter on recovery and rehabilitation. Academic neuropsychology should provide a scientific foundation for clinical neuropsychology, but the two disciplines often fail to connect. 6

7 What is a Clinical Neuropsychologist? Career paths in neuropsychology. Psychology degree. MSc/PhD General clinical training (DClinPsy) Academic research in cognitive neuropsychology. What can brain damage tell us about normal cognition? Specialist training Division of Neuropsychology Membership (MSc + clinical log) Clinical Practice Clinical research What are the most useful methods of assessment & therapy? 7

8 Common causes of acquired brain damage Head injury Stroke Alzheimer s Disease Brain tumour Parkinson s disease Multiple sclerosis Viral infections (encephalitis etc.) 8

9 Head injury = traumatic brain injury The most common cause of brain damage in people under 40. Most head injuries are minor and cause no disability. Causes of severe head injury: 50% road accidents, 30% falls, 10% assaults. But falls are the most common cause for children. The vast majority are closed injuries, not open penetrating injuries Sex & age are the 2 major factors From Kolb & Whishaw 9

10 Head Injury Mechanisms of primary damage. Focal damage under the blow and at the opposite side. A shock wave travels through the brain. Shearing forces forces cause diffuse axonal injury. Bleeding or brain swelling can cause secondary damage 10

11 Head injury sequence of events. Injury Coma/PTA Recovery period Minutes weeks Full recovery or Permanent deficits 6 months Several years 11

12 Head injury defining severity Post-traumatic Amnesia (PTA). Post-traumatic amnesia is the period from injury to the return of orientation for time and place (and therefore includes coma). From Kolb & Whishaw 12

13 Head injury defining severity Coma duration or PTA duration are a (rough) guides to final cognitive outcome. Newcombe, 1987 From Kolb & Whishaw 13

14 Head injury patterns of long-term impairment after severe head injury. Psychological changes are the most evident long-term effects. They cause greater distress than any physical disability. Their incidence is higher with more severe injuries. Brooks et al., 1987 Follow-up of 134 cases of coma > 6hours or PTA > 1 day. Questionnaire interviews with patient and relative. West of Scotland sample with little formal rehabilitation input. Journal of Head Trauma Rehab 2:

15 Brooks et al. (1987). Most common problems reported 2 to 7 years after severe head injury. Problem % relatives reporting % patients reporting Slowness Personality change Poor memory Anger/irritability/impatience Tiredness Tension/Anxiety/Worry Poor concentration Depression Mood changes Poor balance /coordination Some patients lack insight into the extent of their problems. 15

16 Brooks et al. (1987). Most common problems reported 2 to 7 years after severe head injury. Problem % relatives reporting % patients reporting Slowness Personality change Poor memory Anger/irritability/impatience Tiredness Tension/Anxiety/Worry Poor concentration Depression Mood changes Poor balance /coordination Some patients lack insight into the extent of their problems. 16

17 Brooks et al. (1987). Predicting outcome. PTA is a guide to outcome, but there are exceptions:mean rating for forgetfulness = 2/10 when PTA < 8 days and 4/10 when PTA>60days, but 9% are said to have no problem. Level of burden perceived by relatives relates more to psychological changes than to any physical disability Low burden High burden Physical Behaviour Emotional disability Change Change 17

18 Overview on Head Injury The commonest cause of brain damage in younger people. Cognitive problems are the most frequent long term disability, together with behavioural and emotional changes. A large part of work in clinical neuropsychology is dealing with the assessment and rehabilitation of these problems. 18

19 Stroke Brain damage caused by failure of blood supply to the brain. Most common in older people, but there is no lower age limit. Brain haemmorhage is the commonest cause of stroke in younger people. 19

20 Middle cerebral artery the most common site of stroke. Contralateral weakness (hemiplegia). Dysphasia after dominant (left) hemisphere lesions. Visuospatial problems after non-dominant (right) hemisphere lesions. 20

21 Overview on Stroke The most common cause of adult acquired disability Caused by interruption of blood supply to the brain Most (but not all) stroke victims are over 70. Hemiplegia and dysphasia are the most obvious signs but cognitive and emotional changes also common. 21

22 What are the goals of neuropsychological assessment? Contributing to Diagnosis Guiding counselling or rehabilitation. Impossible to predict functional problems directly from brain scans. Neuropsychological assessment is crucial in identifying deficits and spared functions. Monitoring recovery or deterioration. A significant degree of recovery occurs over the months after non-degenerative damage (head injury, stroke). Deterioration in degenerative conditions may be slowed by medical treatments (e.g. drugs in AD). Need for serial neuropsychological assessments. 22

23 What are the goals of neuropsychological assessment? Contributing to Diagnosis Presence of brain damage is now diagnosed by brain scan. Continuing importance in differential diagnosis e.g. dementia or depression? PTSD or head injury? (see Goldstein & McNeil Ch 1) :- 23

24 What are the goals of neuropsychological assessment? Differential Diagnosis - Head Injury or PTSD? 25 yr old man had been in a traffic accident 6 months earlier. His close friend was killed. Initially referred by GP because of complaints of anxiety, irritability, poor sleeping & forgetfulness. CT brain scan was normal. Estimate of head injury severity at interview = mild (PTA<1 hour) but no flashbacks characteristic of PTSD. On a self-assessment questionnaire he rated himself as mildly anxious but not depressed. Neuropsych assessment showed normal visuoperceptual & language skills but mildly impaired episodic memory, processing speed & executive function. Evidence against PTSD - no intrusive thoughts/flashbacks, more severe cognitive problems than explained by mood. Evidence for direct effects of head injury - pattern of cognitive deficits is very typical, despite apparent mildness of injury. Therefore counselling on coping with mild cognitive impairment and advised on graded return to work. Re-assessment in 6 months to monitor expected cognitive recovery. 24

25 Introduction to Clinical Neuropsychology Key Points What is a head injury? What are the most common problems after head injury? What is a stroke? What are the goals of neuropsychological assessment? 25

26 Clinical Neuropsychology. Principles of Assessment Dr Alan Sunderland 26

27 Assessment Tools Interviews, questionnaires and behavioural observation. Normal psychometric tests e.g. IQ scales. Standardised neuropsychological tests. Unstandardised clinical tests. 27

28 Assessment Strategies Traditional test battery approach (e.g. Halstead-Reitan battery, 1940s onwards) Time consuming (all subtests done by all patients). Not guided by theory Use of cut-off scores to diagnose brain damage Single case investigation (informed by neuropsychological theory). Hypothesis testing Sensitivity to specific aims e.g. rehabilitation. 28

29 Neuropsychological assessment. The example of memory impairment. Complaints of forgetfulness are common after acquired brain damage. Why are aspects of memory vulnerable? What have experimental studies told us about the nature of impairment? How should this guide assessment and rehabilitation? 29

30 Using Neuropsychological Knowledge to Guide Routine Clinical Assessment. Evidence from detailed studies of effects of brain damage on memory shows that certain aspects of memory are vulnerable. Much of this evidence comes from unusual cases (e.g. pure amnesia) but it provides a guiding framework for assessing patterns of impairment in more routine cases. 30

31 What principles should guide assessment of memory impairment? Experimental studies suggest: Damage to the temporal lobes (especially the hippocampi) can selectively impair explicit memory for new events. Other aspects of learning and memory may be spared. Memory for verbal and non-verbal material may be differentially impaired. This indicates patterns we should look for in more routine cases where damage is less well defined. And suggests possible areas of strength which may aid rehabilitation. 31

32 The Pure Amnesic Syndrome = severe anterograde amnesia From Kolb & Whishaw 32

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34 The Classic Case of H.M. (1953) Bilateral removal of medial temporal lobes to control epilepsy. A unique case. Bilateral surgery is now avoided. Global anterograde amnesia. Milder retrograde amnesia with temporal gradient. Above average IQ Preserved short-term memory. Preserved implicit memory:- 34

35 H.M. Preserved Implicit Memory Explicit memory = conscious, intentional recollection. Implicit memory = automatic, not dependent on awareness of learning. Procedural learning. Perceptual priming (Gollin figures) From Kolb & Whishaw 35

36 The Amnesic Syndrome Consistent Picture from Case Studies Normal IQ but severe anterograde amnesia. Variable extent of retrograde amnesia ( 0-40 years). Normal short-term memory span. Normal semantic memory (vocabulary etc.). Preserved implicit memory (procedural learning, priming etc). 36

37 The Amnesic Syndrome Implications for Clinical Practice The amnesic syndrome is very rare. But the milder memory deficits commonly seen after head injury tend to follow the same qualitative pattern:normal short-term memory span. Normal semantic memory (vocabulary etc.). Preserved implicit memory. This probably reflect partial damage to the hippocampi in these conditions. 37

38 Medial temporal lobe damage in Head Injury Damage caused by hitting against base of cranium (Sphenoid ridges). 38

39 Material-specific Impairments After Unilateral damage Effects of unilateral temporal lobectomy (Milner, 1967 et seq) Left lesion = impaired memory for words, digits or stories = verbal encoding. Right lesion = impaired for faces, mazes or spatial learning = nonverbal encoding. Clinical effects are typically mild. Not halfway to amnesia. From Kolb & Whishaw

40 Recognition Memory Tests (Warrington, 1986) A widely used clinical assessment. Shown 50 strangers faces & 50 words. 2-alternative forced choice tests Show a double dissociation between impairment for words (verbal) versus faces (nonverbal). 50 Which of these have you seen before? Aid Bake Mean score Controls Left temporal 35 Right temporal Words Faces 40

41 Implications for Clinical Practice. Our knowledge of pure amnesia and effects of unilateral temporal lobe lesions should guide assessment. The following questions should be investigated Is this a selective memory deficit? Measure other cognitive abilities e.g. reasoning ability. Is it limited to longer term episodic memory? Test short term memory and semantic memory. Is this a global deficit? Does it affect verbal and non-verbal material? Is implicit memory spared? Test skill learning and perceptual priming. This systematic approach may allow identification of cognitive resources for rehabilitation. 41

42 Case Example - Neal 17 years old. Traffic accident (bicycle car). In a coma for 17 days (= a very severe injury). No brain damage seen on CT brain scan ( = most damage may be diffuse axonal injury). At 3 months no physical disability. Oriented for time and place but is very forgetful. Aims of neuropsychological assessment: To establish the nature of his memory impairment. To identify cognitive strengths and weaknesses to aid rehabilitation planning. 42

43 Neal. Questions guiding memory assessment. Is this a selective memory deficit? Measure other cognitive abilities e.g. reasoning ability. WAIS-R block design, a nonverbal reasoning test. Age scaled score = 8 Normal for age = 10 +/- 3 But very slow on a 4-choice visual reaction time test. A non-verbal reasoning test So, no severe impairment of reasoning ability but slowed rate of information processing. 43

44 Neal. Questions guiding memory assessment. Is it limited to longer term episodic memory? Test short term memory (digit span) and semantic memory (Graded Naming). Normal digit span = 7 forwards. Graded Naming Test Age-scaled score = 10 Average for his age group. So short-term memory & semantic memory are not significantly impaired. Graded Naming Test. Ability to name Objects of increasingly low frequency. Can be used as a test of semantic memory. 44

45 Neal. Questions guiding memory assessment. Is this a global deficit? Does it affect verbal and nonverbal material? Normal ability to draw Rey Figure. But zero recall from memory. Face recogntion = 2 Word recognition = 2 Rey Complex Figure Ability to recall a short story. Immediate recall = 6 Delayed recall = 0 Therefore, a global episodic memory deficit. Recognition memory tests 45

46 Neal. Questions guiding memory assessment. Is implicit memory spared? Test skill learning and perceptual priming. Improves performance with practice. Suggests intact skill learning. There are no good standardised tests of implicit memory. 46

47 Summary of Neal s Assessment His deficit follows the pattern of global amnesia It is not as severe as HM or other pure amnesics. But he does have the additional cognitive problem of slowed information processing. His intact reasoning ability, semantic memory, and skill learning can be mobilised in his rehabilitation. 47

48 Conclusion on assessment in clinical neuropsychology Hypothesis-guided case investigation as the best approach. The example of memory impairment shows how cognitive neuroscience can inform routine assessment. This may identify resources for rehabilitation. 48