A CLINICAL PHILOSOPHY

What distinguishes the clinical neuropsychologist from the neuropsychologicaltechnician is adherence to the scientist–practitioner model.

The history of this model, promulgated for decades in many branches ofpsychology, was reviewed by Benjamin and Baker (2000). It requires that psy-chologists become trained both as scientists and practitioners. Some branchesof neuropsychology have grasped this approach. In fact, the model is almostinherent in the very title of the subject. The best clinical neuropsychologistscontinue to refine the relationship between neurological knowledge and clini-cal practice. Assessment should not be an isolated event but involve whereverpossible engagement with other professionals concerned with the case.

The term ‘clinical’ is used rather loosely in a wide variety of areas in neu-ropsychology. Certainly, many who use the word in their professional title or inprinted works show little evidence of what might be termed a clinical philoso-phy. With the enormous growth of postgraduate courses in neuropsychologythere is a now a wide divergence in modes of practice, which, in turn, may berelated to the efficiency of such practice. This effectiveness will depend onseveral factors. The principal of these might be termed clinical insight.

It is obvious that individuals with similar professional qualifications canvary widely in this insight or clinical acumen, that is the ability to synthesizeall aspects of the case into a probable diagnosis or hypothesis. Though difficultto achieve it would be helpful to be aware of the presence and degree of suchability in selecting candidates for training in a clinical area. The issue of train-ing clinicians concludes the final chapter. Without such selection criteria atten-tion must focus on maximizing the potential both of those in training and thosealready in practice.

The central issue concerns a difference between the capacity to acquire infor-mation and the ability to utilize it. In his classical 1954 text, Clinical Versus StatisticalPrediction, Paul Meehl commented: ‘. . . but to come to the hypothesis may requirespecial dispositions on the part of the clinician which are only acquired by experi-ence superimposed on what may or may not be a fundamental personal talent’. 395

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The teachability of such a general hypothesis-forming disposition is, of course, animportant problem that has hardly been investigated at all.

The ability is possibly made up of a number of separate attributes so that thetotality will vary from individual to individual. Some apparently intelligentindividuals, such as university lecturers, even those with an encyclopaedicknowledge of an area, may have a paucity of generative abilities. One of these,we believe, is tolerance of uncertainty or ambiguity. They are uncomfortable ifthey cannot achieve what some psychologists term ‘closure’ over a problem.Another talent is the ability that one might term pattern perception, the capac-ity to recognize a Gestalt compounded from a variety of components. Nocumulation, however detailed, has the significance of the whole. There areobviously other traits that make for an effective clinician.

As in some medical schools, our own method of increasing the value ofclinical experience lay not so much in the number of cases but of case presen-tations by the trainee examiner to a critical audience and, even more impor-tantly, by requiring trainees to write a detailed case report, which forced themto examine their own thought processes about the way that they had pro-ceeded. Unlike some battery approaches, trainees were encouraged to performthe process in stages where, after broad hypothesis-testing they were encour-aged to have periods of cogitation or discussion with others before selectingmeasures for the next stage until they achieved what in psychological diction-aries is called the ‘aha experience’, the feeling that accompanies the momentof insight when the disparate elements come together. This is not a fully con-scious process and many times we awake with a solution that was not therethe night before.

CLINICAL APPLICATION

Before outlining a particular approach to clinical appraisal considerationshould be given to the nature and limitations of many tests and the role offactors that are likely to affect their use.

Care with quantification

Though well-developed psychometric measures possess some clear assets theyneed to be treated with care in the clinical setting.

A common difficulty arises with tests employing summarizing measures.These indices may bury the very data that is of significance in understandingthe patient’s difficulties (see Lezak 1988, Walsh 1991). One could call this the sinof summation.

While measures such as IQ or MQ can be very useful in examining normalsubjects they can be misleading in clinical cases. A subject may obtain aMemory Quotient above 120 on the Wechsler Memory Scale, an apparentlysuperior memory performance. However, in some cases the subject may showby consistent failure of all ‘hard’ items of the Associate Learning subtest thatthey have a severe new learning or amnestic disorder, which is confirmed bythe clinical history substantiated by extended testing.

The same logic extends to the summation of items within a test.

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In both cases certain critical item or subtest failures of key significance canbe obscured. A classical example in pseudoneurological cases is the failing ofeasy items accompanied by passing on the more difficult, although thesummed score is ‘within normal limits’ or ‘fails to meet the cutting point’. Insuch cases failure on simple problems is most unlikely to be due to neural inca-pacity and raises the possibility of role enactment. For detailed examples seeBinder and Pankratz 1987, Pankratz 1979, 1983, Pankratz et al 1987, 1975,Pankratz and Paar 1988, and Walsh 1991.

If one invokes the simple notion that the difficult subsumes the easy, thencombined scores mean that this key to understanding of the individual casemay be lost. Internal consistency with regard to item difficulty is an importantelement of the interpretation of test performance.

Finally, a summary score may lead some to assume that it has the same sig-nificance in the neurologically impaired as it has in the intact subject. For exam-ple, two equally gifted individuals sustain head injuries. After the acute phaseone individual tests higher on an intelligence scale leading some to believe thatthe prospects for rehabilitation in that case are better. However, the individualwith the higher score has features of the dysexecutive or frontal syndrome, ren-dering occupational rehabilitation difficult or impossible, while the individualwith the lower score does not have such features and can be rehabilitated,albeit at a lower level of work than before.

Care with face validity

There is a danger in assuming that if a patient fails on a particular test then thatpatient must have a deficiency in the psychological function stated by the man-ual to be what the test measures. However, ‘most tests have only an indirectrelationship with the variables they are supposed to measure’ (Shapiro 1973).

A simple example of making the wrong inference might be as follows: thepatient produces a poor score on a memory for designs test, e.g. the BentonVisual Retention Test (BVRT), and this is then reported as a ‘visual memorydeficit’ and this may be extended to the further inference that ‘the patient showspoor visual memory suggesting impairment of the right hemisphere’ or evenmore specifically ‘the patient shows differentially poor visual memory with nor-mal verbal memory suggesting impairment of the right temporal region’.However, in the form given the memory for designs test may have relied on thepatient drawing the remembered stimulus. Thus one of the possible reasons forfailure could be an executive or graphic difficulty, i.e. the reason for failure is thesame as the reason the patient fails on other tasks with a constructional element.Awareness of such a possibility would prompt the use of a task where the con-structional element has been removed, e.g. The Multiple Choice version of theBVRT. Here the subject is shown a design and then must select it some time laterfrom a multiple-choice array, which contains the item plus three distractors. Thesame logic applies, mutatis mutandis, to the examination of other possible causesfor poor performance, e.g. perceptual difficulties.

In summary, many tests are multifactorial in their composition and hypothe-ses about the possible reasons for poor performance need to be examined. Thisprocess may involve the use of other tasks, but may also be solved by notingthe performance of the subject on tests already performed. The multifactorial

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determination of test scores is one of the stumbling blocks of deriving infer-ences from group data since ‘Different individuals may obtain the same testscore on a particular test for very different reasons’ (Ryan & Butters 1980).Miller (1983) nicely refers to the process as ‘paralogical thinking’. He cites onestudy which argued that since normal elderly subjects did less well on teststhat have been shown to be sensitive to right hemisphere pathology, the righthemisphere ages more rapidly than the left. He emphasizes that while a lesionlocated at a particular point may produce a test deficit, this does not mean thatthe converse follows. ‘In fact the logical status of this argument is the same asarguing that because a horse meets the test of being a large animal with fourlegs that any newly encountered large animal with four legs must be a horse.The newly encountered specimen could of course be a cow or hippopotamusand still meet the same test’ (Miller 1983, p. 131).

Further examples of incorrect inferences are given in Walsh (1995).Conversely, multiple failures on seemingly disparate tests with different

named functions may reflect a common disorder. The magnitude of the failureon separate tests will be a reflection of the degree to which the disturbed func-tion is represented in their composition. In most situations only a small num-ber of functional disturbances will account for the many observed deficits inperformance on a plethora of tasks. In attempting to explain them it is wise toremember that the law of parsimony has never been repealed.

Determinants of performance

Another shortcoming of studies relates to the principle of multiple determi-nation. ‘Behavioural deficits are defined in terms of impaired test perform-ance. But impaired test performance may be a final common pathwayfor expression of quite diverse types of impairment’ (Kinsbourne 1972).Smith (1975) commented about a commonly used test, the Digit–SymbolSubstitution Test, in similar vein, `the responses are the end product of theintegration of visual perceptual, oculomotor, fine manual motor and mentalfunctions’. It is therefore important to be aware that low scores on such com-plex tasks may be due to a disturbance in any of the functions involved or anycombination of them.

If complex tests must be used, two methods of clarification are possible:(i) to observe the sharing of variance between a patient’s performance onsundry tests; and (ii) to test hypotheses about the various possible reasons forfailure (see below). In the latter instance the practitioner will be helped by asound knowledge of the corpus of knowledge in neuropsychology.

Closely allied to the notion of multiple determination is that of multiplepathways to the goal. Many psychological tests are concerned solely withwhether or not the subject can reach the goal. ‘The flexibility of cerebral mech-anisms is such that the solution of most test items can be reached by many devi-ous routes. The method the subject uses in tackling a problem will in generalprovide more information as to the character of a skill or of a psychologicaldeficit than will the knowledge as to the subject’s success or failure’ (Elithorn1965). Qualitative observations are of paramount value and no amount ofquantification will, at times, override the importance of the psychologist as anobserver of behaviour.

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Symptoms and syndromes

The significance of a patient’s symptoms and signs can be understood inthe context of the notion of a functional system (Ch. 1). A functional systemin the brain consists of a number of parts of the brain, particularly but notexclusively cortical, together with their fibre connections. The system operatesin a concerted manner to form the substratum of a complex psychological func-tion. This systemic concept allows a new approach to the use of psychologicaltests in the diagnosis or assessment of neurological conditions, an approachwhich parallels the study of other bodily systems.

It will be apparent that if a psychological process is served by an anatomicalsystem, which is spread out in the brain, then the psychological process will bevulnerable at a number of different points, some of which may be widely sep-arated. Such a finding was, in fact, one of the seemingly powerful argumentsused against the early localizationists. If, for example, speaking or writing orperceiving could be altered by lesions in sundry locations, then these functionscould not be localized. The argument turns, of course, on what is meant by‘localized’.

The modern notion of a functional system also incorporates the notion ofregional specialization within the system and it is this which increases its valueboth in theoretical explanation as well as application to the individual case.While damage anywhere in the system will lead to some change in the functionthat the system subserves, the nature of the change will be dependent upon theparticular part of the system that is damaged or the set of connections that hasbeen disrupted, since each part contributes something characteristic to thewhole. It is thus necessary to look carefully at the nature of the changes in apsychological function to determine how they are related to the location andcharacter of the lesion.

This multiple significance of what appears at first to be the same symptomor symptom complex begins to render meaningful the apparently conflictingfindings of many early studies and, at the same time, allows symptoms or signsto have localizing value. To take a common example, psychologists have longobserved that the Kohs block design test is often performed poorly by many,but certainly not all, brain-impaired subjects. Poor performance on this testcould result from a disruption of what might rather loosely be termed con-structional praxis. It could also be performed poorly because of visual andother difficulties but if these are excluded and poor performance of the blockdesign task is taken as an operational definition of constructional apraxia, theregional significance still remains to be determined. Here qualitative observa-tions are of help. For example, constructional deviations where the patient failsto conform to the square framework are observed most strikingly in patientswith posterior lesions, particularly right-sided. Constructional deviations areparticularly prominent in right-hemisphere lesions and markedly so wherethere is a posterior locus.

An equally poor score on the block design test may be obtained by a secondpatient with a frontal lesion. However, such a patient will usually show fewconstructional deviations and the difficulty may be shown to be dependentupon incomplete preliminary investigation of the problem as in the case exam-ined by Luria and Tsvetkova (1964) cited in Chapter 4. In this case the frontal

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patient is helped by the provision of a design card upon which the outlines ofthe four (or more) constituent blocks have been drawn. On the other hand,right parietal patients tend to benefit little from such a procedure. The ‘partiallysolved’ block design problem apparently has no more meaning in theirshattered visuospatial world than the original.

The neuropsychological syndrome

Deriving as it does largely from the broad base of clinical neurology, the con-cept of a syndrome plays a central role in the thinking of clinical neuropsy-chology. Central to the concept of the syndrome is the sense of a uniqueconstellation of signs and symptoms, which occur together frequently enoughto suggest a particular underlying process. However, not all the signs andsymptoms are of equal importance and the weighting of the different elementsis often an idiosyncratic process ‘being unformulated outcome of the inter-action of medical instruction and clinical experience’ (Kinsbourne 1971).

Neuropsychologists should be concerned with the pattern of impairmentand as their knowledge of syndromes increases they will, when confrontedwith certain symptoms and signs, look for the association of the other featuresto confirm or disconfirm the presence of a particular syndrome. This is themedical model of differential diagnosis.

For the method to work effectively in clinical practice, knowledge is required inthree areas: (i) the corpus of fact in human neuropsychology; (ii) an acquaintancewith relevant principles and details of allied clinical neurosciences especially clin-ical neurology, neuroanatomy and neuropathology; and (iii) psychological testtheory and practice.

Syndromes also vary a good deal in their degree of specificity or vagueness.The frontal lobe syndrome is a much more general working term than, say, thegeneral amnesic syndrome. One of the reasons for this generality may be thegrouping together of a number of functionally different areas, particularly ifthese are affected simultaneously by one pathological process. However, if theterm syndrome is used in an extremely broad sense then it fails to have mean-ing. One such usage was the earlier term ‘chronic brain syndrome’.

Finally, it is essential to stress that it is the total configuration or Gestalt thatimparts significance. A syndrome is, indeed, more than (or other than) the sumof its individual constituents. It is useful working fiction, which allows us tocreate some order out of the complexity of the patient’s subjective complaintsand the findings of our examinations. Knowledge of a variety of syndromesallows us to generate hypotheses about the nature of the disruptions offunction in the individual case.

The method of extreme cases

Training in differential diagnosis is best done by what Kraepelin called ‘themethod of extreme cases’ (Zangwill 1978, personal communication). Thetrainee neuropsychologist should be introduced to syndromes in their clear-cutform, i.e. classical or ‘extreme’ cases. Later, more subtle and complex cases canbe introduced to teach the range of variation that might be encountered in clin-ical practice. We have found that this method facilitates the recognition of

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syndromes in their less dramatic or latent forms and makes it possible to detectcharacteristic patterns of neuropsychological deficit in their early stages ofdevelopment. Such early detection can be critical in certain disorders.

HYPOTHESIS TESTING IN THE SINGLE CASE

History

The development of hypotheses springs first from data gathered before theexamination. In 1975, Hampton and colleagues showed that: ‘Extra time spenton the history is likely to be more profitable than extra time spent on the exam-ination’ (p. 489). The history is particularly important where time availablewith the patient is limited.

Lezak (1980) stressed the necessity of considering the examination in whatshe nicely termed the ‘multidimensional contextual framework’. This back-ground would include the educational and social history, the medical historyincluding prior professional opinions, and the circumstances leading to thepresent evaluation. Ideally, the data should be available for cogitation for sometime. Unfortunately, it is not always to hand before the evaluation, the patientsometimes presenting with a brief ‘letter of referral’.

A good history also requires the neuropsychologist to have a significantgrasp of allied disciplines such as neurology and psychiatry, otherwise crucialfactors will be overlooked. In most cases temporal aspects of the disorder mustbe included. In many instances, it is absolutely essential that a careful historybe taken from a spouse, other relative or caregiver, not only for elaboration butto detect differences in historical accounts. In many neurological disordersaffecting cognition, the patient may be unaware of the reasons for referral, thetrue nature of the disability or its consequences, nor able to describe thechanges in behaviour. On the other hand, in many psychiatric or psychologicalconditions the patient is painfully aware of perceived deficits, which do notaccord with objective performance.

In recent times heavy reliance on solely technological advances has set atrisk the interpersonal relationship, particularly dialogue, with the patient. Thisis a retrograde step since the most important information in deriving hypothe-ses often comes from data that only the patient can provide.

Qualitative information

One serious drawback to almost every purely quantitative approach to neuro-psychological evaluation is the loss of information. Shapiro (1951) quotedSchafer: ‘A test response is not a score; scores, where applicable, are abstrac-tions designed to facilitate intra-individual and inter-individual comparisons,and as such they are extremely useful in clinical testing. However, to reason –or do research – only in terms of scores or score patterns is to do violence to thenature of the raw material. The scores do not communicate the responses in full’(emphasis added). Reitan’s (1964) study, mentioned in Chapter 4, shows clearlythat, utilizing the same test data, clinical prediction can be superior to formal orpsychometric methods. This may have been due to loss of qualitative features

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in individual responses or complex intra-individual patterns of response lostwhen only levels of performance were used. More recently Goldberg and Costa(1986) restated this truism: ‘The behavior that generates scoreable responses is,however, far richer and more varied than any scoring system will allow’. Whileit is desirable to use quantification wherever possible, some clinically relevantinformation does not lend itself readily to such quantification.

One way of coping with the limitations of scores alone is by recording thequality and patterning of responses noted during evaluation, ‘informationabout the neuropsychological processes which underlie a subject’s perform-ance can only be provided by a detailed qualitative analysis’ (Ryan & Butters1980). This position is supported in the approaches of Kaplan and her col-leagues (Kaplan 1988, Kaplan et al 1991) where task- or process-specific samplequalitative responses are provided in the test material.

Hypothesis testing

Shapiro has also pointed out some of the major difficulties and limitationsinherent in the application of standardized validated tests in the clinical diag-nostic setting. These comments remained pertinent and, after two moredecades, Shapiro was still able to point to the absence of any serious attemptsin the intervening period to overcome these difficulties by application of therecommended solution, namely the experimental investigation of the singlecase (Shapiro 1973). After reminding us of the scientific concept of error in psy-chological measurement, Shapiro argued that while this should prevent usfrom making unwarranted generalizations from the data it should not preventus from using observations in a systematic way to advance our understandingof the individual case.

The awareness of error makes us look upon any psychological observationnot as something conclusive but as the basis of one or more hypothesesabout the patient. One’s degree of confidence in any hypothesis suggestedby an observation would depend upon the established degree of validity ofthat observation and upon other information about the patient concerned.If one or more hypotheses are suggested by an observation, then stepsmust be taken to test them. In this way further observations are accumulatedin a systematic manner. It should then become possible to arrive at apsychological description in which we can have greater confidence. Theadditional observations may in turn suggest new hypotheses which havein turn to be tested. We are thus led to the method of the systematicinvestigation as a means of improving the validity of our conclusionsabout an individual patient. (Shapiro 1973, p. 651)

Working hypotheses may arise from generalizations that have emergedfrom the research literature. Clinical neuropsychology is becoming very rich inthis regard as evidenced by the samples provided in Chapters 4 to 9, which,while representative, is far from exhaustive. As this work grows, converginglines of evidence make the generalizations more secure and thus facilitate theimplementation of crucial tests of the various hypotheses, e.g. the evidence onasymmetry of hemispheric function has made the testing of laterality of lesionsmore open to systematic investigation.

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Despite his forceful advocacy, even Shapiro considered that this methodmight not have strong appeal since it could tend to be time consuming. In prac-tice, however, it tends to be more economical than the application of a fixed bat-tery of tests, since many of these prove irrelevant to the questions being asked.Since in clinical practice certain questions tend to recur frequently, traineesquite soon recognize the most likely hypotheses and the most productive teststo be used in particular situations. Subsequent case evaluation in the light ofneurological or neurosurgical knowledge continually improves the process.

In busy clinical practice, time is an expensive commodity and on some occa-sions the clinician has to tender an opinion after less than an ideal examinationof the patient. In this situation the report should make it clear to the referringsource that the opinion consists ‘of the hypotheses which the applied scientistthinks best account for the data at his disposal, and which he would choose totest next time if he had sufficient time and suitable means’ (Shapiro 1973,p. 652). The term ‘suitable means’ often takes the form of appropriate tests. Insome cases these do not exist but this situation has become uncommon as neu-ropsychology has developed and clinicians working in a particular field arelikely to acquire the tests that prove useful in answering the most commonhypotheses. Data from subtests of such well-established measures as the WAIS-R or the Wechsler Memory Scale may well provide the central hypothesis,which can then be tested by other procedures. Sometimes the whole or part ofthe answer lies in testing that has already been carried out with standardizedtests. Psychologists well versed in psychometric practice may not be aware thatmuch of the information for clinical decision making is already availablethough not recognized through lack of training.

As referring agencies become more sophisticated neuropsychologically, theyare more likely to present quite specific hypotheses for investigation. This islikely to result from the appreciation of well-written reports. The followingexample from the companion volume (Walsh 1991) illustrates such a referral.The neurologist wrote: ‘Does this patient have an amnesia to which she is notentitled?’ Though not expressly stated the neuropsychologist is being asked tostudy the patient’s hospital file. Perusal of this record revealed the following:A 56-year-old housewife had a history of episodes of sudden detachment fromreality, staring eyes and lack of awareness of her surroundings, each episodelasting about two minutes. The episodes had commenced shortly after a headinjury 15 years before, when she was struck on the right temple. EEG record-ings had consistently shown the presence of a left temporal focus with no elec-trical abnormality on the right side. All attempts to control the attacks withdrug therapy had failed and the patient was proposed as a candidate for leftunilateral temporal lobectomy. Depth electrodes strongly confirmed thepresence of a left medial temporal focus. It was at this stage that the referralquestion was put.

The question, thus placed in its context, assumes that the neuropsychologistis familiar with the literature related to the question. The neurologist will not besurprised if the patient shows a differentially weaker verbal than non-verbalmemory performance in line with the proven double dissociation shown withlateralized temporal lobe lesions between verbal and non-verbal material. Thiswould be a deficit to which the patient would be ‘entitled’ by virtue of a leftmedial temporal lesion. However, a ‘non-entitled’ deficit of non-verbal memory

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would signal a possible dysfunction in the right temporal region. This dysfunc-tion might be silent to neurological examination since in the case of an atrophiclesion, the area may be electrically silent, i.e. a normal EEG on the right sidewould not exclude pathology.

The import of finding a non-entitled neuropsychological deficit would havethe utmost significance since surgical ablation of the electrically active focus inthe left temporal lobe would be added to the atrophic damage in the previouslyunsuspected right side. Functionally, this would be equivalent to bilateralmedial temporal damage, a condition that produces a general, profound andlasting amnesic syndrome. Hence, the finding of an amnesia to which thepatient was ‘not entitled’ would be a clear contraindication to surgery.

In this case the neuropsychological examination did show minor difficultywith one aspect of new verbal learning though verbal short-term memory,memory for prose material and other verbal intelligence measures were at anappropriate level. However, the patient clearly had much more difficulty withnon-verbal memory together with evidence of constructional dyspraxia due tomore widespread right-hemisphere disruption of function. It seemed that theproposed surgery ran the risk of producing a general amnesic syndrome. Atthis stage the patient died suddenly and at autopsy the site of the left-sided irri-tative focus was of normal appearance while the electrically silent right sidewas atrophic in the hippocampal region. To operate would have been to pro-duce a devastating amnesic disorder.

Selecting the tools

Knowledge of syndromes and brain–behaviour relationships will be the prin-cipal factor in determining the selection of tools. Certain of these will beemployed on an almost daily basis in answering commonly occurring ques-tions. However, there will be questions or hypotheses that will require ‘special’tools, which will produce pathognomonic data. Test selection should be ger-mane to the questions asked, so that the experienced neuropsychologist willgradually develop quite a large armamentarium from which to choose. Thereis now a large number of texts giving extensive detail on many useful tests. Theclinician will add a personal store of further qualitative observations. Such testfamiliarity is necessary for the rapid and economic evaluation associated withthe branching decision-making process, which is the basis of clinical evaluationusing a flexible or individualized method. In the case extracts that follow onlya few well-known tests are cited but this is merely to exemplify the way inwhich assessment can proceed.

The selection of tests may entail a one-step process, i.e. a group of tests ischosen in the belief that these will provide the information needed to answermost questions. Sometimes the issues will remain unresolved but observationsderived from the primary set of tests may suggest that further specific testsmay provide the answer, i.e. a stepwise approach will be used by many. Muchof the efficacy of this method turns on the selection of the primary group oftests, since the use of tests that do not touch the problem at all will give appar-ently negative results. In reporting such negative results it is important toinform the referral agency that ‘nothing abnormal was detected with the testsused’. It is of help to colleagues familiar with psychological tests to specify

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exactly which ones were used. These should certainly be documented in hos-pital practice and in medico-legal cases. Unfortunately, negative reports areoften written, which contain the implication that no impairment is present. Weshould bear in mind Teuber’s dictum ‘absence of evidence is not evidence ofabsence’ (of impairment). Russell (1982) pointed out that the entire controversybetween fixed versus flexible test methodology hinges on a single rather obvi-ous principle that is axiomatic to neuropsychology: ‘one cannot determinewhether a certain function of the brain is impaired unless that function is tested’.

REPORTING

Reports should be written primarily for the referring source preferably being freeof technical terms not widely known. They can not only record the neuropsychol-ogist’s findings but can be conveyed in a way that could increase the understand-ing by other professionals of the settings in which neuropsychology can be useful.Clearly written reports should contain a description of the patient’s performancefollowed by conclusions and, where relevant, the arguments used in support ofsuch conclusions. They should comment not only on the qualitative and quantita-tive findings but also on such matters as the congruence between similar measuresof the same function and congruence between test performance and reportedbehaviour. A chart of numerical data is appropriate as an addendum, especially inthe records of clinics and hospitals where the report may be read by practitionersin related fields or subsequently by other neuropsychologists. Finally, the reportshould not move beyond the neuropsychologist’s areas of expertise, e.g. to com-ment on matters best addressed by another professional such as a neurologist.

This process may appear time-consuming but proves helpful in forcing theexaminer to exteriorize thinking processes, thus leading to further develop-ment of clinical competence. The sequential nature of the problem-solvingprocess with neurobehavioral disorders often means that brief verbal inter-changes with professionals in related fields will modify the next step in theinvestigation procedures of both parties leading to economy of time and effort.For further detail see Walsh (1991, 1992, 1995), and the forensic neuropsychol-ogy section in Chapter 11.

Lastly, we are a long way from developing robust tests for use in relationto competence in daily living activities necessary for rehabilitation. Currentneuropsychological tests do not cope with the amalgamation of the numerouscomplex functions necessary for concluding many everyday tasks.

CASE EXAMPLES

In applying the hypothesis method to ‘clinical’ cases neuropsychologists willencounter different types of situation. Commonly they are asked to confirm thelikelihood that the features presented by the patient or client represent aparticular disorder or syndrome. This is commonly the case in referral frommedical or psychologist colleagues.

On other occasions the matter is presented as a puzzle or problem for whichan appropriate hypothesis is sought. In such situations the neuropsychologist

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needs to generate a number of possible explanations or hypotheses and testbetween them.

Finally, the neuropsychologist may become involved in deciding betweenopposing hypotheses being put forward (often very strongly) by different par-ties as is often the case in medico-legal disputation (see Ch. 11). This latter sit-uation offers an excellent opportunity for expounding the advantages of theproposed philosophy of evaluation. The first two cases are typical examples.

In recent times clinical neuropsychology has moved increasingly towardsunderstanding the nature and degree of functional disturbance rather thanregional diagnosis, though this role continues to be an important contributionparticularly to neurologists and neurosurgeons.

Choosing between hypotheses

Head injury or alcohol-related damageCASE: NG

This 45-year-old marketing executive was severely injured in a motor vehicleaccident in which the driver of the other vehicle and two passengers werekilled. On arrival at a small town hospital some 30 minutes after the crash NGwas unconscious and did not regain consciousness for another four hours, butremained confused and required sedation for three days. Radiological exami-nation revealed a fracture of the maxilla and a fractured humerus but no skullfracture. Imaging was not available. Neurological examination showed nolocalizing signs. A week after the event NG was transferred to a metropolitanrehabilitation centre where he was found to be correctly oriented but mildlydisinhibited. CT scan at ten days after injury was unremarkable and the patientwas considered fit for discharge home by the end of three weeks.

Personal History. The patient’s past history was elicited from him and frommembers of his family. He had a master’s degree in business studies and was amember of the board of his company. His family commented that he nowseemed less reserved than before and on several occasions had made crude com-ments, which were atypical for him. He was described by himself and his fam-ily as a social drinker, consuming on average about four or five standard drinksa day, and only exceeded this on rare occasions such as family celebrations.

At later interviews some three and four months after injury NG’s wife andson both commented spontaneously on his ‘personality change’, which theydescribed as a brashness and marked lack of sensitivity that was in contrast tohis pre-accident state, and they mentioned that he had alienated many of hisformer friends and colleagues. His wife was concerned by the resulting isola-tion but it appeared not to concern NG.

He returned to work at four months and coped with his work adequatelythough he now made errors that he not made before and was intolerant of crit-icism. His firm moved him to a less-demanding position and one where he hadfewer dealings with clients. A promotion, which was about to be given at thetime of his accident, was deferred.

About two years after the accident NG was referred for neuropsychologicalevaluation in support of a claim being made that he had suffered changes dueto brain impairment as a result of the event. It was learned that opposing legalargument centred on the position that any changes observed in NG were due

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to alcohol-related brain damage, a position supported by opinions given by apsychologist and a psychiatrist who had examined him several times in theperiod dating from 18 months to two years after the event.

At interview, NG admitted to the neuropsychologist that he was aware thathe had changed but showed incomplete insight into the effect theses changeshad on others. He admitted that he did not seem as good at his job as formerlybut could not explain the difficulty and tended to play this down.

Neuropsychological examination. Several examinations were conducted inthe period from one and a half to three years after the accident. His perform-ances were stable over these examinations. The WAIS results shown are takenfrom an examination two years after the accident by the psychologist who hadoffered alcohol as the cause of any deficits that the subject might have.

The principal hypothesis suggested by the history was that the clinicalchanges seemed characteristic of closed head injury affecting the anterior por-tions of the brain. Since the personality changes alone appeared almostpathognomonic, the examination was designed to confirm the hypothesis byevaluating aspects of adaptive behaviour with appropriate and sensitive meas-ures described in the literature (see Ch. 5, Walsh 1991).This was imperative,since an alternate cause, namely alcohol-related brain damage, had beensuggested by a psychiatrist and supported by a clinical psychologist.

Milner pathway on the Austin Maze Test (Walsh 1991). Several examinations overtime showed essentially the same pattern. The following represents the examina-tion at two years. Over the first ten trials NG reduced his errors consistently.

Nevertheless, he continued to make errors on further trials, even after hehad achieved two (non-consecutive) errorless trials. He appeared only mildlyfrustrated and applied himself saying that he was keen to succeed.

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WAIS scaled scores

Information 13 Picture Completion 14

Comprehension 13 Object Assembly 10

Arithmetic 12 Block Design 12

Digit Span 12 Digit-Symbol 13

Similarities 14 Picture Arrangement 12

Vocabulary 13

VIQ 119 PIQ 126

Full Scale IQ 124

Trial 1 2 3 4 5 6 7 8 9 10

Errors 15 6 9 5 5 4 3 3 2 1

Trial 11 12 13 14 15 16 17 18 19 20

Errors 2 1 6 4 0 2 1 1 1 0

Trial 21 22 23 24 25 26 27 28 29 30

Errors 2 2 1 2 1 1 1 1 1 1

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This is a classical pattern whereby patients with anterior damage from what-ever reason find it difficult if not impossible to eradicate all errors from theirprogrammes of behaviour to produce a stable error-free performance (Walsh 1991).Moreover, he made different errors on different occasions, cursing mildly andchiding himself when he did so.

Tested again at three years he made only one error on the third trial but over30 trials was never able to gain more than two successive error-free trials.

Rey figure. The copy was complete but the recall at three minutes wassparse (Fig. 10.1).

He also recalled two features but stated that he did not know where theyshould be placed in the whole and was asked to draw these in the margins ofthe paper. The performance seemed characteristic of those patients with frontalpathology.

Verbal fluency. He managed to average only 11 words for the three letters(F-12; A-7; S-14), which would place him just below the 25th percentile, con-siderably below expectation based on his educational and social history and hisfluent use of language in normal conversation and his score on the Vocabularysubtest of the WAIS. He also broke the rules several times though he was ableto repeat these rules when asked. This did not prevent him from breaking themagain subsequently.

Tower of London (Shallice 1982, 1988). The first four problems were solvedquickly. He solved problem five slowly and seven only when he insisted on‘having another try’ and failed on item six and the final four items. In discus-sion after the task he made quite intelligent comments about how to achievesolutions demonstrating the frontal ‘dissociation between knowing and doing’(see Ch. 4).

Trail making test. Part A was performed accurately and rapidly (25 seconds)but he was considerably slower on Part B (119 seconds), though he made noerrors.

Colour–Form sorting test. He spontaneously announced the two principlesof ‘shape’ and ‘colour’ but then sorted immediately according to form and did

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408 Fig. 10.1 Case NG. Recall of Rey Figure at three minutes.

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so again. When asked what he was supposed to be doing he spontaneouslymade the shift to colour. Once again he seemed to show a mild dissociationbetween conceptualization and action or ‘inability to shift’ as described in theearliest literature on frontal lobe damage.

On this test his performance seemed close to expectation. After 30 minutesdelay he recalled nine of the ten pairs in the Associate Learning subtest. He wasthen given the Rey Auditory Verbal Learning Test (RAVLT). This consists offive learning trials of a 15-word list followed by one recall and one recognitiontrial after a single trial of an interpolated list of the same length.

This performance seemed below expectation for an obviously intelligent manand, again, he seemed unable to perfect his learning. From the 2nd to the 5th trialboth the order of responses and the missing words differed from trial to trial.

Discussion. In general, the severity of closed head injury has been relatedto the length of the period of unconsciousness or preferably to the period ofpost-traumatic amnesia (PTA) (see Walsh 1991, Ch. 5). The longer the period ofPTA, the more likely it is that the person will have lasting deficits. However,while this generalization is clinically useful there are exceptions, e.g. somecases with relatively short periods of PTA have demonstrated radiologicalchanges of considerable damage particularly in the frontal regions and theseinvariably reveal deficits of personality and cognition (Levin et al 1989).

From the scanty records this man appears to have been unconscious for a fewhours and confused for approximately four days. His wife said that his memorywas poor for at least ten days, but this estimate came over one year later.

General argumentHead injury. It is not unusual to see preservation of high scores on standard

psychometric measures following head injury in formerly intelligent subjects.

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WMS Form I

Information 6 Digits Total 12 (7,5)

Orientation 5 Visual Reproduction 14

Mental Control 9 Associate Learning 11 (6,2; 6,3; 6,4)*

Memory Passages 11

MQ 122

*Note: The designation (6,2; 6,3; 6,4) refers to performance on the learning of the 10 pairs of theverbal paired associate learning task where six pairs have logical associations requiring therelearning of old associations (e.g. baby – cries) and four pairs require the learning of novel asso-ciations (e.g. crush – dark). Thus a perfect score would be ‘6,4’. In the case YW, presented below,the scores (5,0; 6,0; 5,1) are quite typical of verbal–specific or general amnesic syndromes, and thepatient shows a marked dissociation between the ‘old’ and ‘new’ learning.

RAVLT

List A List B List A List A

Trials 1 2 3 4 5 Recall Recall Recognition

Correct 8 12 13 12 13 7 10 15

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This does not signify preservation of ‘effective intelligence’ since the disordersof adaptive ability, which are so debilitating in these patients, are not revealedexcept in severe cases. Intelligent individuals develop numerous programmesof behaviour that allow them to deal with a wide variety of everyday situa-tions. On the other hand, they have difficulty both in generating new pro-grammes for behaviour and adapting prior programmes to meet changingcontingencies.

NG did show the consistent and characteristic learning and executive diffi-culties described in those with anterior brain damage (Austin Maze, ReyFigure, Tower of London, RAVLT). These features accompanied personalitychanges, particularly disinhibition of the type reported almost invariably withtrauma to the frontal parts of the brain. The present patient was indifferent tohis own errors and the effect of his behaviour on others. Both sets of changesappeared for the first time immediately after the injury and there was noevidence of attempts to exaggerate or enact other deficits.

The alcohol impairment hypothesis. Features which militate against this are:(i) none of the observed changes of personality or cognition were reported byany observers to be present before the injury, even in retrospect – changes withalcohol-related brain damage are slow and insidious, never of sudden onset;(ii) the type of change in personality is uncharacteristic of alcohol-related brainimpairment but highly characteristic of traumatic damage; (iii) while changesin adaptive behaviour and problem solving largely dependent on cognitiveloss are a feature of alcohol damage – they occur against a background of morewidespread cognitive deterioration – in all cases in our experience thesechanges lead to a lowering of some subtests of the Performance Scale, in par-ticular Object Assembly, Block Design and Picture Arrangement (for examplessee Walsh 1991, Ch. 2); (iv) while it is often difficult to gain a true estimate ofthe degree of an individual’s drinking, there was no evidence of the usual sortput forward even by those supporting this hypothesis, i.e. prolonged heavydrinking (often combined with inadequate nutrition); and (v) mild atrophy,which had been seen in the CT scan, might be consistent with alcohol damageas well as traumatic damage, but there was also a localized area in the front ofthe brain more consistent with trauma though, of course, head injuries are verycommon in alcoholics.

The court ruled in favour of head injury as the cause of the man’s changes.Certainly the post hoc ergo propter hoc argument is strong in such cases,especially if evidence can be produced of absence of deficits in the periodimmediately prior to the event.

A second case of head injury(Courtesy Dr Marie O’Shea)CASE: XX

This 31-year-old bank teller sustained a minor head injury when a car beingdriven by a relative struck him as he stepped onto the driveway of the familyhome. He was thrown to the ground striking the left side of his head. He didnot lose consciousness and there were no discernible periods of retrograde oranterograde amnesia. He was examined in the emergency department of a cityhospital and, with the exception of a graze above the left eye, sustained noother apparent injuries, and was discharged home. Four days later XX attended

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hospital for a routine cardiology review for a congenital heart condition thathad necessitated multiple cardiac operations in the past and a life-long relianceon warfarin therapy. At that time he complained of persistent headache andhad a peri-orbital haematoma and a left subconjunctival haemorrhage, whichhe felt was spreading. In view of the recognized risk of cerebrovascular com-plication after head trauma in someone on warfarin (a blood thinning agent) aCT scan was performed and reported as normal and he was discharged to thecare of his general medical practitioner. He returned to work a week after theaccident but had to leave work four days later due to persistent headache andnausea. Later that evening he was found unconscious in bed by his wife andsubsequently suffered a generalized seizure. An ambulance was called and herequired intubation at the scene. An urgent CT scan on admission showed alarge right subdural haematoma and a fracture of the base of the skull. Heunderwent immediate surgical evacuation of the subdural collection. A repeatCT scan four weeks later was unremarkable apart from evidence of previousischaemia in the right internal capsule thought to have occurred much earlier.He was transferred to a rehabilitation centre where he remained for threemonths and attended as an out-patient for a further 12 months.

Personal history. Mr XX completed 11 years of formal education anddescribed himself as an ‘average’ student but did not seem confident with thisassessment. He repeated a year due to hospitalization for his cardiac condition.On leaving school he completed a clerical course but could not succeed with anaccounting course. His working life has been spent as a bank teller. Despiteseveral attempts he could not attain promotion.

A four-month work trial with the bank starting six months after the accidentwas unsuccessful. He felt that the trial was going well and his hours wereincreased. He was subsequently informed that he was not suited to branchwork. He could not write as well, his memory was not as efficient, and he wasphysically restricted. He, however, felt that he was given inadequate trainingwith respect to new products and was hence unable to cope. A short time laterhe successfully completed two computer courses but these did not translate toemployment. He eventually obtained work as a part-time car-park attendant.He was otherwise the primary carer of his three young children allowing hiswife to return to full-time employment. He managed the household finances,gardening, home and car maintenance, whilst his wife attended to the house-hold chores. He maintained an interest in the local football competition and hissocial activities were unchanged.

Neuropsychological examinations. His first evaluation was three monthspostinjury. His subjective complaints included some memory difficulties, irri-tability, and a lack of motivation. On assessment, he was said to show ‘signifi-cant cognitive difficulties encompassing a range of cognitive domains’. Thesame neuropsychologist reviewed him 12 months postinjury at which timehe denied any ongoing cognitive or behavioural changes. Of significance, hiswife corroborated this account. On formal examination, however, it remainedthe opinion of the neuropsychologist that, despite improvement, Mr XX‘continued to display significant cognitive difficulties [consistent with] amoderate to severe generalized brain injury’.

This examiner’s interpretation of the neuropsychological profile seemed to bepredicated on the assumption that XX sustained a significant head injury with the

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complication of a ‘subarachnoid haemorrhage’. By contrast, the history was infact one of a relatively mild head injury and the vascular complication was a rightsubdural haematoma. The distinction is a significant one, and one which shouldbe known to properly trained neuropsychologists. Different pathologies result indifferent neuropsychological outcomes. Subarachnoid bleeding may destroyneural tissue while pressure from subdural bleeding may disrupt function of theunderlying tissue without destroying it. Surgical relief of this pressure may resultin major or complete restoration of function. In addition to this, poor perform-ance in domains well known for their resilience to acquired cerebral insult (e.g.fund of general knowledge) were being attributed to the recent medical history.The neuropsychologist also failed to address the incongruity between the appar-ent severity of cognitive deficits outlined on formal examination and spousereports of no significant change.

About three years after the accident XX had a third evaluation in the contextof a personal injury claim. Based on one scale of the WAIS-III (i.e. PIQ) andusing ‘best subtest’ performance as a benchmark, the neuropsychologist con-cluded that XX was likely to have been a person of average premorbid ability.(For a critique of this approach of estimating premorbid functioning seeMortensen et al 1991, Franzen et al 1997). Against this background, he was con-sidered to display a difficulty with complexity on tasks such as the PacedAuditory Serial Addition Task often used in measuring recovery from concus-sion. Since such measures are also related to numerous factors, poor perform-ance cannot necessarily be taken as evidence of acquired cerebral damage.

In the context of an ongoing medico-legal claim in the adversarial system,a fourth evaluation was requested by opposing counsel. This took place fouryears following the trauma. At that time, the client’s complaints of residualphysical disability were restricted to some mild right-sided weakness forcingincreased reliance on his left (non-dominant) hand and the wearing of a braceon his right leg. He did not volunteer a cognitive complaint. When specificallyquestioned about this he described a minor inefficiency in his thinking such asoccasional forgetfulness and reduced concentration. In addition, he gave anaccount of a moderate disturbance of mood but without evidence of a primaryalteration of personality or behaviour. With the evidence of a clinically evidentdepression and longstanding mild speech impediment his presentation wasotherwise unremarkable.

Examination of his general intellectual ability at this time employing WAIS-III yielded the following summary quotients: Verbal IQ = 84; Performance IQ =85; Full Scale IQ = 84. Such findings placed abilities in the ‘low average’ rangeof the scale. Direct comparison with the earlier evaluations confirmed stabilityof the VIQ and PIQ with some improvement in the overall FSIQ. A number offactor-based Index scales were calculated as follows:

A discrepancy analysis revealed no statistically significant differencebetween the first two, verbal versus non-verbal cognition. By contrast, working

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Verbal Comprehension Index 82 (low average)

Perceptual Organization Index 74 (borderline)

Working Memory Index 88 (low average)

Processing Speed Index 106 (average)

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memory function was significantly better than his non-verbal performance andhis processing speed better than all other indexes. Since working memory andspeed of function are two of the domains most vulnerable to injury this wasthought to be an important consideration. The integrity of these functions wasconfirmed by the application of several other specific tests.

Close inspection of the WAIS subtest details suggested that despite acquir-ing a fund of general knowledge within the ‘average’ range, his vocabularywas modest. This was accompanied by a restricted ability to identify abstractrelationships in language. Arithmetic ability was also poor with the nature ofhis errors indicative of a poor understanding of more complex mathematicalprinciples. A similar level of variability together with a rigid cognitive stylealso characterised his non-verbal performance. Whilst variability is often con-sidered to be a reflection of acquired change this is the case only if it makes‘neuropsychological sense’. In this case, the pattern of variability was more inkeeping with a longstanding cognitive profile.

To more directly examine the issue of acquired intellectual change versus alongstanding pattern the Wechsler Test of Adult Reading (WTAR, Wechsler2001) was given. There were no statistically significant differences between theactual IQ scores and those predicted by the reading test.

A similar comparison between attained versus predicted performance onthe WAIS factor-based index scales showed only one difference, namely that ofthe Processing Speed index which was better than predicted. Qualitative exam-ination of subtests was unremarkable.

Similar procedures were carried out with regard to memory with the sameoutcome.

Memory function was further examined with other tasks. The BVRT was‘average’ for one of his intellectual background. His reproduction of the ReyComplex Figure Test was well planned and spatially accurate and recall after abrief delay was consistent with his age and other factors. Similarly his per-formance across the acquisition, interference and delay conditions of the ReyAuditory Verbal Learning test were ‘low average’ consistent with his generalverbal abilities.

In another area he reported moderate levels of depression on the BeckDepression Inventory and severe levels of anxiety on the Beck AnxietyInventory although the latter was inflated more by his concern with physical asopposed to psychological conditions.

Discussion. Considerable debate occurred amongst various examinersregarding the client’s premorbid level of functioning and the related issueof acquired impairment. The psychological literature contains up-to-date

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VIQ PIQ FSIQ

Actual WAIS-III score 84 85 84

Predicted WAIS-III score 79 83 78

Immediate memory General memory Working memory

Actual WAIS-III score 96 96 91

Predicted WAIS-III score 84 87 86

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information on various tests used as predictors. One psychiatrist using theNelson Adult Reading Test (1982) estimated XX’s premorbid intellectual abilityto be at IQ around 95. This test tends to over-estimate premorbid IQ at lowerlevels and under-estimate the figure at higher levels. Utilizing one of the cur-rent formal measures of premorbid ability (WTAR), which has been specificallyco-normed with the intellectual measures employed, no significant discrep-ancy was disclosed between either Mr XX’s current general intellectual abilityor his performance in more discrete cognitive areas including memory.

Of further relevance was the pattern of performance across specific meas-ures with his best being in the spheres of psychomotor speed and workingmemory. Since these are well known to be most vulnerable to trauma this ishighly significant.

The basic question is: what level of impairment might have been suspected?The head injury was minor. The complication was that of a delayed onset sub-dural haematoma. As mentioned earlier a rapidly and successfully treatedsubdural haematoma is not necessarily accompanied by a long-term impair-ment of cognitive or behavioural function. There is little doubt that there wasdisruption of neuropsychological function in the early recovery period(although it is probable that the severity of this deficit was over – interpretedat the time of the initial neuropsychological evaluations). Careful analysis overtime indicates that in fact he made a good neuropsychological recovery.

Some examiners attributed an organic basis to XX’s personality features. Thereports of family members suggested that his general personality was little alteredfrom his premorbid nature. It was likely, however, that depression, anxiety, andfrustration relating to his physical restrictions and altered life circumstancesfollowing the accident (and its complications) has led to some reactive changes.

This case was settled out of court on agreement being reached that Mr XXhad indeed made a generally good cognitive recovery. The neuropsychologicalargument helped in achieving this result.

Functional versus organic

Neuropsychologists may be asked to clarify the degree to which neurologicalor psychological factors contribute to a patient’s behaviour. Both the followingcases urge caution about being dogmatic in early evaluation.

Two examplesCASE 1: WN

A 53-year-old woman was the caretaker of a house that caught fire. Although noserious damage occurred the incident was upsetting for the ‘house minder’. Oneweek later WN was having dinner when she experienced a five-minute period ofchest pain with nausea together with five minutes of difficulty in enunciating herwords. She also complained of weakness of her left upper limb, which persisted,and some hours later her friend took her to hospital where the examining neu-rologist felt that this might represent a right-sided cortical event. The neurologistalso felt that there were few signs consistent with organic impairment and sev-eral suggesting that the weakness of her left hand could be either ‘functional’ orpsychologically based. The neurobehavioural examination included a request todraw a bicycle. Her attempt is shown in Figure 10.2. The drawing was rudimen-

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tary and included the dotted figure as an afterthought. She described the figureas ‘a man who puts one leg on each wheel’.

With an ‘hysterical’ disorder as a possible diagnosis, the neurologist alsoadministered the 15-item Memory Test of Rey. (The stimuli for this test areshown in Fig. 10.11). The patient’s first response was to continue the alphabetin columns of three underneath the correct first line A B C and, when shownthe stimuli again and asked to reproduce them from memory a few secondslater, she began with the number one and continued the numerical series untilstopped by the examiner.

Because of the possibility of a non-neurological basis of her difficulties a psy-chiatric opinion was sought five days after the event. It is noteworthy that aCT scan taken soon after admission was reported as being within normal limits.

There was no previous psychiatric history. She was described as being alert,cooperative, attentive and correctly oriented. She did, however, evince errors inspeech and perseveration. She was able to give internally consistent details ofher background and history and at this time told the examiner of how therecent fire had brought to mind a tragic event of her childhood when at the ageof five or six years her younger brother of some two years was burned to death,an event that she had witnessed.

The psychiatrist commented that her disorganized mental state appeared tohave a considerable functional element, but he also felt that an organic causefor her left arm weakness needed vigorous investigation.

After a further few days she was noted to have no difficulty speaking, but theweakness in her left hand persisted. The neurologist on that occasion admittedthat he could not decide whether her problems were ‘functional or organic’.

About a week after admission the speech pathologist described her as hav-ing non-specific speech and language problems most consistent with frontallobe pathology sparing the major language areas. However, she said that shecould not rule out a functional element. The major signs included persevera-tion, poor self-monitoring, difficulty in learning new material, reduced verbalfluency with inappropriate responses and verbal paraphasias.

The neurologist was puzzled by this case and sought advice from theDepartment of Neuropsychology. On seeing her drawings, which included theComplex Figure of Rey done two days after admission (Fig. 10.3), and hearingthe story, the neuropsychologist suggested a number of tests, the first one of whichwas the Colour–Form Sorting Test, an extremely simple but rewarding task.

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415Fig. 10.2 Case WN. Drawing of a bicycle.

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The examination was videotaped and shown to the consulting neuropsycholo-gist who pointed to the presence of all the qualitative features that have beenshown on this test by patients with frontal-lobe pathology. The patient also showeda poverty of response on the Verbal Fluency Test and the characteristic features

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416Fig. 10.3 Case WN. A, Copy; and B, Recall of the Rey Figure two days after admission(order of drawing is indicated by solid lines followed by progressively more broken lines).

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shown on such tasks by patients with left or bilateral frontal lesions. This con-firmed the findings of the speech pathologist’s earlier examination. Other taskssensitive to frontal pathology, such as the Porteus Maze Test, were performedpoorly. The Rey Figure was again disorganized (Fig. 10.4). The opinion was that thepatient had significant frontal pathology with clear evidence of left-hemisphere

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417Fig. 10.4 Case WN. A, Copy; and B, Recall of Rey Figure seven days after admission.

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involvement and that this could account for all the test findings and the patient’sclinical presentation. The numerous qualitative observations did not support aseparate or additional diagnosis of a functional disorder.

Concurrently with the neuropsychological examination, a repeat CT scanrevealed a left-sided frontal infarct (Fig.10.5). The reason for apparent weak-ness on the ‘wrong’ side, i.e. ipsilateral to the lesion, never became clear. Suchweakness had resolved by the end of one week.

With the emphasis on quantitative measures in much of neuropsychologicalevaluation there is a great need for articles such as that of Goldberg and Costa(1986), which add a rich description of qualitative features that are characteristic ofcertain types and locations of pathology. By far the most effective way to conveythis material to trainees is by videotape but such material is unfortunately sparse.CASE 2: SA

The patient was a 40-year-old science graduate who had successfully workedon research projects for some years before taking up administrative posts inwhich he was described as capable and efficient. However, he was without ajob after his position was made redundant in an economic recession and he wasstill without work when he was seen a year later.

His wife and his father described changes in his personality around thistime. He had become withdrawn and largely uncommunicative. This was amarked difference from his prior outgoing, gregarious character.

Two separate psychiatric examinations could find no typical disorder. A trialof antidepressant medication made no difference to his state. He was thenreferred to a neurologist whose examination revealed no abnormal clinicalsigns. The neurologist noted that he was unable to elicit any ‘complaint of cere-bral disarray’ from the patient whom he described as ‘most unforthcoming’.The neurologist was sure that all was not well and thought that a tumour ordegenerative process should be investigated. The latter possibility was

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418 Fig. 10.5 Case WN. CT scan showing wedge-shaped infarct.

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strengthened when the neurologist talked to SA’s father, who described ‘anobvious deterioration in mental sharpness and in the élan of his conversationand social address to family, friends and acquaintances’ over a year or more.He was then referred to a neuropsychologist for diagnostic help.

Neuropsychologist A was a very experienced clinician and at initial inter-view he confirmed that SA was reticent and appeared to have no insight intothe changes already described. SA said his wife got upset at times because,‘I eat too much and am a bit lazy’.

Tests used comprised four subtests of the WAIS-R, WMS Form 1, TrailMaking Test, Rey Figure, Verbal Fluency, and the Austin Maze.

This examiner commented that he was unable to find reproducible evidence ofintellectual or memory decline. The patient performed normally ‘on tasks notedfor their sensitivity’ including the maze test. He believed that ‘the questions raisedby the man’s general presentation were not supported by the neuropsychologicalfindings’. However, certain disparities were noted. For example, despite his back-ground, SA stated that water boiled ‘at 110˚F or about 40˚C’. His arithmeticalresponses were cavalier and impulsive. Although his prose recall was excellent, onAssociate Learning he ‘exhibited a rapid learning of the material then a suddenforgetting of it’. He was said to have no difficulty with the verbal fluency task.

Doctor A was puzzled at the lack of signs and asked colleague B for a sec-ond opinion. This was done some four weeks later. Details of the first exam-ination were not yet to hand though the history and the essence of the report tothe neurologist had been given in discussion between the two neuropsycholo-gists. B decided to repeat the interview and to repeat the maze test to observethe patient’s behaviour until the earlier results were to hand. Parts of thesecond report read:

This man presents a subtle problem. To my surprise, as soon as I met himI felt there was something neurological in the wind. I was quite astounded,knowing his past history, to find him both fatuous and vacuous. Hisconversation was almost devoid of content, and the further we went in theinterview the more apparent it was that he had absolutely no insight intowhat must be quite considerable changes in him over the last year or more.His responses to my few pleasantries seemed excessive. As at formerinterviews, he stated blandly that there was nothing amiss with him andpassively accepted any suggestion I put to him without the slightest show ofaffect. At the same time, I was tolerably well convinced that he was in no waydepressed and, in one sense, I would not even describe him as apathetic.

It seemed to me that he was like patients I have seen with frontal lobedegeneration of an extensive kind and the old truism came to mind thatsuch patients may appear essentially normal until you sit down and testthem, that is, with appropriate tests. Of course, I was then confronted withthe verbal report I had been given about some of his test performances,which might seem at first to make the hypothesis unlikely.

Nevertheless, I thought it would be helpful to repeat at least theAustin Maze and to push it a bit further. To my increasing surprise, hegave a quite classical frontal performance . . . He demonstrated that hewas familiar with the rules by answering my queries correctly and,concentrating well, he reduced his errors to only one after seven trials but

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took another seven to reach his first error-free performance. However,unlike the previous occasion with Dr A only a month before he thenimmediately reverted to making an error. Even when I stopped him andasked him where he was going wrong, he was able to indicate the placewithout difficulty but then repeated the identical error five times beforereaching another error-free trial. (Errors: 8, 7, 5, 8, 3, 2, 1, 2, 1, 2, 2, 1, 2, 0,1, 1, 1, 1, 1, 0 . . . discontinued.)

There was now no doubt in my mind that he was showing the classical‘dissociation between knowing and doing’ together with the problem oferror utilization pathognomonic of frontal lesions.

The hypothesis that had been growing in B’s head since hearing the historywas receiving support. The examination was then deferred until A and B coulddiscuss the previous results. Many would have gone ahead and given a repeatseries of tests.

This review brought out some features not inconsistent with the hypothesis,which B stated as DFT, or dementia of the frontal type.

The Verbal Fluency result was thought to be very poor for SA’s backgroundand the richness of his responses on the Information subtest. He also madethree rule-breaking errors.

A low score on arithmetic was the result of failing on the last three itemsthrough impulsive errors.

Having acquired three of the four difficult pairs on the Associate Learningsubtest, he lost them on the next trial despite the fact that he appeared to beattending and cooperating with the examination.

Arrangements were being made for further examination when the patientleft the area. However, at this time a CT scan revealed atrophic changes in thefrontal regions with mild enlargement of the frontal horns of the lateral ventri-cles. It is important to note that an EEG and a neurological examination werenormal.

Six months later, although his symptoms had worsened, SA cooperated wellenough with a third examiner at another hospital to complete some tests, e.g.WMS-MQ 114.

A further six months later the same neuropsychologist described him asrestless and he sometimes stood up to do the tests and wandered in and out ofthe room. Nevertheless he managed to complete some tasks.

His MQ had fallen to 89 but, as before, his visual reproduction was verygood. Though he managed only three subtests his performance score wasaround 94 (previously 105 six months before and 117 a year before).

This psychologist commented: ‘On the Picture Completion subtest he was ableto name quite complex items that were missing and this was unusual in someonewho had performed so badly elsewhere. On the Block Design subtest he gave upafter the sixth item but prior to that he had done some quite quickly and man-aged others with a little encouragement. He had to be constantly pushed to dothe tests. He did the Object Assembly items very quickly. He was quite unreflec-tive; he just rushed in and put things together, but basically he managed to getthem correct and obtained his best score at a near average level’.

This neuropsychologist believed that there had been ‘a very significantdeterioration’ but SA did not have any disorder of visual perceptual or

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constructional skills. She commented: ‘What seems to be lacking is the abilityto regulate, to monitor, and to check what he is doing in a normal manner.Throughout, he seemed to have the ability to continue with a task once he hadstarted going on it, but then when he gave up or stopped, he could not self-direct back to it’.

About this time repeat CT scan showed an increase in the frontal atrophynoted earlier with ventricular enlargement, prominence of the Sylvian fissures,and other features seen in Pick’s disease.

Progress. The major signs of blunted affect, poverty of speech, lack ofinsight, restless wandering, and disinhibition (such as undressing in public)gradually worsened and he was hospitalized in a closed psychiatric centre.There had been no response to antipsychotic medication. Despite this progres-sion, SA remained oriented.

Neurological examination was still essentially normal but some primitivereflexes had emerged.

This case is a prime example of the old adage that you only diagnose whatyou know. The second examiner had seen other cases before.

A medley of case extracts

The following medley may serve to exemplify a few of the range of questionsasked of neuropsychologists. The extracts are of necessity brief. In each case thepresented data is restricted mostly to a few widely known tests. Often manyother tests were employed. It is difficult to do justice to even the most straight-forward case in a brief span, but each case has a point to make. As such expe-rience accumulates the clinician develops an ever widening and consolidatingframe of reference against which to make future judgments.

Korsakoff psychosisCASE: YW

A year before his assessment, YW, a 49-year-old teacher, had suffered a ‘nerv-ous breakdown’ when he was unable to remember certain commitments ashead of a rural school. Soon after hospitalization a CT scan revealed cerebralatrophy, a diagnosis of Korsakoff psychosis was made, he was hospitalized fortreatment of his alcoholism and had been abstinent since that time.Neuropsychological assessment was requested as part of the decision as towhether he might be able to return to work or whether he should be retired.

YW began drinking in his early twenties and gradually increased his con-sumption of beer on a daily basis in the rural towns where he spent his profes-sional life. He had never appreciated that he was drinking to excess andmanaged to obtain higher teaching certificates over the years. He was neverabsent from work until the final episode, which brought him under attention.At this time he was consuming more than two litres of wine per day.

He presented as an alert cooperative man, well aware of his condition overwhich he showed realistic concern. He said that he was strongly motivated toreturn to work but knew that his memory was poor though somewhatimproved since be became abstinent. He wrote down everything that he had toremember, but there was no evidence of how effective this strategy had been.He had been abstinent for several months at this examination.

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The Wechsler Memory Scale (WMS) and the several subtests of the WechslerAdult Intelligence Scale (WAIS) immediately revealed the extent of hisdifficulties.

This revealed the features of a general amnesic syndrome. YW was well ori-ented, though confused on questions of current political leaders. In keepingwith preservation of insight into his deficits he showed no confabulation.Automatic mental operations were performed speedily without error andimmediate memory span was normal. However, there was a clear anterogradeamnesia (Memory Passages, Visual Reproduction, Associate Learning).

The amnesic difficulty was strongly confirmed by the RAVLT.

YW performed a little better on the fifth trial than many with alcohol-relatedmemory deficits, but considerably below that expected from his background.The results also show a characteristic retroactive inhibition or interferenceeffect shown by a score of only three after the interpolated list. He also showedinterference by intruding words from the previously administered associatelearning subtest. As with most Korsakoff patients, the recognition trial wassignificantly better than any of the recall trials.

The complex Figure of Rey showed a very good copy, followed by anattempt at recall, which rated a score of zero when the patient attempted todraw the figure from memory only three minutes later (Fig. 10.6).

An indication of YW’s premorbid intellectual ability can be gained from thethree verbal subtests. These would suggest a prior level in the vicinity of 130IQ. In contrast, the two tests requiring planning and problem solving weresignificantly inferior. On Block Design he showed inappropriate strategiesattempting to solve the problems using faces of the blocks having only onecolour, rotating them at odd angles to achieve a diagonal effect. There wasalso a disinclination to alter placements that he clearly recognized as being

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WMS Form I

Information 3 Digits Total 13 (7,6)

Orientation 5 Visual Reproduction 8

Mental Control 9 Associate Learning 9 (5,0; 6,0; 5,1)

Memory Passages 4.5 (5,4)

MQ 94

RAVLT

List A List B List A List A

Trials 1 2 3 4 5 Recall Recall Recognition

Correct 5 7 8 8 11 5 3 14

WAIS scaled scores

Information 12 Digit Symbol 12

Comprehension 18 Block Design 8

Similarities 14 Object Assembly 7

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incorrect. He was, however, upset with not being able to succeed on tasks thathe knew would clearly have been well within his ability.

Three months later another examination was requested before the final deci-sion was taken on his re-employment or retirement. No measurable improve-ment had taken place and the testing was terminated when he becamedistressed after failing totally to make the slightest improvement after ten trialson the Milner pathway of the Austin Maze Test.

This case not only illustrates most of the commonly found features of analcohol-related disorder, but also shows how advanced cognitive deficit maybecome in certain situations before action is prompted.

YW shows a general amnesic syndrome together with other non-amnesiccognitive deficits. These latter have been termed ‘the adaptive behavioursyndrome’ (Walsh 1991) and may predate the emergence of an amnesicdisorder by years or may be seen without amnesia in the well-nourishedalcoholic.

Amnesia complicating arteriographyCASE: DD

Following an adverse reaction to angiography at another centre this 54-year-old accountant was admitted to the emergency ward in a semi-comatose con-dition. Over the preceding eight weeks he had suffered a number of suddenattacks of dizziness and incoordination with weakness of the left arm and leg,each attack lasting two to three minutes. On occasion he also reported numb-ness of the left side of the face. Apparently the examining physician felt thatcarotid arteriography was indicated but, for reasons that never became clear, avertebral injection was made instead and a large dose of contrast material was

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Fig. 10.6 Case YW. Recall of Rey Figure at three minutes.

Austin Maze (Milner Pathway)

Trial 1 2 3 4 5 6 7 8 9 10

Errors 19 10 15 17 11 19 15 15 23 15

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used. Shortly after the injection the patient lost consciousness for a few minutesthen roused sufficiently to realize that he was blind. He was confused andshowed retrograde amnesia for events over the past few days. Neurologicalexamination revealed no other localizing signs but it was apparent that DD alsohad a severe anterograde amnesia. At this stage he was transferred to a largemetropolitan hospital’s department of neurology. As with idiopathic cases oftransient global amnesia (without blindness) he continually posed the samequestions about what had happened to him. Over the next 12 hours he slowlyimproved but was confused, irritable and disoriented and constantly com-plained of poor vision but was unaware of his recent episode of blindness.

The first neuropsychological examination was carried out 18 hours afterangiography. By this time he was able to distinguish objects and could describea person at four feet (1.22 m). His memory had improved sufficiently for himto recall an interview with the psychologist, which took place one hour before.The Wechsler Memory Scale was administered at this time and comparisonsare given when he was re-examined at 72 hours and four weeks after the event.

At 18 hours. Performance on the WMS suggested a general amnesic syn-drome, though it was difficult to interpret the poor performance on VisualReproduction because of the patient’s visual problem. Associative verbalfluency was given but he was able to give only two words on the letter F in 60seconds and zero on the letters A and S. He was able to read words, andname objects and colours and showed no other difficulties.

At 72 hours. This examination showed marked improvement in DD’smemory. The improvement in Visual Reproduction was confirmed by theBVRT where he scored seven correct out of ten with only four errors. Despitethis, DD’s recall of the Rey Figure fell to only eight, three minutes after he hadscored 32 out of a possible 36 for his copy. His vision had returned to normalbut he was very anxious about the possible return of his blindness. Onceagain he found it very difficult to find words according to their beginning let-ter. He managed only four for F, five for A, and seven for S, despite a VerbalIntelligence Quotient (WAIS) of 131, and he had had much difficulty with thepaired associate learning subtest of the WMS. His memory weakness ham-pered his acquisition of the Milner pathway on the Austin Maze Test wherethere was no significant reduction of errors from the third to the eleventhtrial. In sharp contrast, DD’s performance on the Spatial and LogicalArrangement Tasks of Lhermitte (see Walsh 1991, Appendix) were performedperfectly on the first trial. There were no conceptual difficulties on severalother tests.

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WMS Form I 18 Hours 72 Hours 4 Weeks

Information 6 6 6

Orientation 3 5 5

Mental Control 9 8 9

Memory Passages 6 12 10

Digits Total 13 15 15

Visual Reproduction 1 10 11

Associate Learning 7.5 (5,0; 5,0; 5,0) 10 (4,0; 6,1; 6,1) 14 (6,0; 6,3; 6,2)

MQ 89 122 132

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At 5 Days. CT scan revealed no evidence of cerebral infarction.At 4 Weeks. Further improvements were shown though, once again, his dif-

ficulty with paired associate learning was apparent and he managed to reachonly the 40th percentile on the word fluency task, a considerable deficit for avery intelligent man as shown by an extended examination. The parallel formof the Rey Figure (Taylor Figure) was recalled almost perfectly after threeminutes. Finally, as it was considered that there was still some verbal memorydifficulty the RAVLT was given.

This was thought to be well below par and the poor recognition memorywas somewhat surprising.

DD had returned to work and was not concerned about his memory butremained very apprehensive about having another attack of blindness and wasstill concerned over this when he visited the hospital a year later with anotherunrelated complaint.

Amnesic strokeCASE: XD

This successful businessman was 65 years old and had been in good health untilsix months prior to his admission. He had suddenly became blind while drivinghis car but stopped the vehicle without mishap. The blindness was total butresolved after ten minutes. During this time XD noted difficulty with his memory.

Following this episode XD suffered many attacks of blurring of vision,associated vertigo and memory loss lasting 15 to 30 minutes. Although heimproved greatly after each attack he felt that there had been a general deteri-oration in his memory and he had become very tired in recent months.

Neurological examination revealed no observable deficits and no carotidbruits were noted. The clinical history prompted angiographic examination.The main abnormality was a very hypoplastic right vertebral artery and asmooth walled left vertebral with a gross stenosis at its origin. There was alsoa plaque on the right internal carotid artery.

Neuropsychological examination was requested prior to vertebral endarterec-tomy since poor vertebrobasilar perfusion appeared to be the likely cause ofhis troubles.

On examination he was alert, oriented and cooperative, with a clear insightinto the presence of his stable memory disorder.

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RAVLT

List A List B List A List A

Trials 1 2 3 4 5 Recall Recall Recognition

Correct 8 11 13 9 11 6 9 4

WMS Form I

Information 4 Digits Total 9 (6,3)

Orientation 5 Visual Reproduction 5

Mental Control 9 Associate Learning 6.5 (3,0; 5,0; 5,0)

Memory Passages 2

MQ 87

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There was no confabulation despite the extreme poverty of his verbal recalland on the second card of the Visual Reproduction subtest he failed to gaineven one point. The RAVLT showed the same features as in the preceding caseof the general amnesic syndrome, though much more severe, namely, pooracquisition, retroactive inhibition and good recognition score.

A perfect copy of the Rey Figure was followed by a much impoverishedrecall at three minutes with only the basic outline retained (Fig. 10.7).

Sundry subtests of the WAIS showed the patient to be in the normal tobright normal range with no qualitative features suggestive of deficit otherthan the amnesia.

Re-examination. Five weeks after endarterectomy XD was re-examinedwith parallel forms of the tests given before operation. There was no change ineither direction and added memory tests only served to confirm the presenceand severity of the amnesic disorder.

A final examination after the lapse of another six months showed the condi-tion to be stable. XD was anxious and frustrated because of the pervasivenature of his memory loss coupled with retention of full insight into his condi-tion. He had suffered no further attacks of visual difficulty and his visual fieldswere normal.

The silence of the right frontal lobeThe following case illustrates that there is at least one area of the brain whereextensive damage may take place without significant change emerging on thewide range of cognitive tests currently employed in neuropsychological assess-

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RAVLT

List A List B List A List A

Trials 1 2 3 4 5 Recall Recall Recognition

Correct 4 4 4 4 7 4 0 15

Fig. 10.7 Case XD. Recall of Rey Figure at three minutes.

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ment. The following résumé covers only part of the detailed investigation ofthis case.CASE: WS

WS was a 14-year-old student who was admitted to hospital with multipleinjuries when a home-made bomb he was constructing exploded with a devas-tating result. He remained conscious despite a penetrating wound above theright eye into the cranial vault, a penetrating chest wound, a penetratingabdominal wound with protruding bowel, lacerations to the hands and minorinjuries to the legs and genitalia.

Among numerous emergency surgical procedures, fragments of bone andmetal were removed from the right frontal lobe though other fragments remaineddeep in the lobe (Fig. 10.8). The extent of damage can be gauged from this scan.

WS remained conscious, alert and orientated most of the time. Apart from theprimary surgery, a mediastinal abscess was later drained together with a peri-cardial effusion. Despite these harrowing experiences, WS was able to be movedto a general ward only two weeks after admission. At this time he was grosslyuninhibited in a fluctuating manner, at times being polite and accommodating,and at others grossly uncooperative, abusive, manipulative and carrying outnumerous unsavoury acts such as throwing faeces at the staff. This behaviourmoderated sufficiently over the next two weeks to enable efforts at rehabilitationto commence, though he lacked motivation and varied in his concentration span.His first neuropsychological assessment was carried out three weeks after hisadmission. Because of his many injuries, which caused pain and discomfort, anda tendency either to fatigue or to become bored, the examination was carried outin several short sessions. Each time he was pleasantly cooperative, though flat inaffect, and at times mildly adynamic. At other times he was easily distracted.

By this time it was known that WS had had a long history of an antisocialconduct disorder though little detail was to be obtained from the parents who,however, felt that there had been little personality change since the explosion.

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Much of the poor performance on the three items from the PerformanceScale was due to slowness resulting from lack of dexterity secondary to hishand lacerations. A minor analytical difficulty was apparent on the BlockDesign subtest.

No suggestion of memory deficit was seen in this excellent set of perform-ances, which was commensurate with his VIQ.

Corsi block tapping test. Immediate memory span: 8.Complex figure of Rey. A complete but somewhat careless copy was made

which was well planned. At this stage WS appeared bored and his poor recallwas difficult to interpret.

Austin Maze (Milner pathway). WS enjoyed this game-like test, mastering itin only five trials, a very superior performance (for further information seeWalsh 1991). He then insisted on being allowed to try it backwards makingonly one error at his first attempt and zero on his second. Next day he asked todo it again with exactly the same result. Complex learning of this type wasclearly unaffected.

Tower of London test (Shallice 1982). This was included in a series of testsusually shown to be sensitive to left frontal lobe damage since it was possiblethat damage might have been sustained in areas other than the primary site ofimpact. Here again WS turned in a first-rate performance:

Several other tests suggested intact cognitive processes at a level in keepingwith his above-average intelligence.

When seen at five months postinjury, extensive examinations revealed someimprovement in speed of information processing, but an otherwise stable set ofcognitive performances. On the Taylor version of the Rey Figure his recall score

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WISC-R age scaled scores

Information 10 Picture Completion 10

Comprehension 10 Object Assembly 8

Arithmetic 12 Block Design 7

Digit Span 9 Mazes 13

Similarities 12 Picture Arrangement 7

Vocabulary 9

VIQ 114 PIQ 92

WMS Form I

Information 4 Digits Total 10 (6,4)

Orientation 4 Visual Reproduction 13

Mental Control 9 Associate Learning 19 (6,2; 6,4; 6,4)

Memory Passages 11 (13,9)

Average preparation time 5.7 seconds

Average execution time 11.5 seconds

Correct 10 of 12 correct with 3 errors, two of which were recognized and corrected

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reached the 100th percentile. The analytical problem on the Block Design itemswas still in evidence but only on the most difficult items.

Unfortunately WS was still causing concern because of his antisocial con-duct. He still retained his old group of friends and mixed well with his peergroup. It was impossible to tell whether his psychosocial difficulties had beenexacerbated by his injuries. His mother at this stage described him as ‘a deviantlittle brat’ who had not been worsened by the event.

Alcohol and error utilizationCASE: ZS

This man had always worked as an unskilled labourer and had a long historyof alcohol abuse dating back at least 20 years. His own (possibly conservative)estimate was at least 12 standard drinks per day. His alcoholism had caused thebreakdown of his marriage seven years before and he was reduced to relyingon charitable institutions for lodging and support. At this stage he realized thathe needed professional help and entered a recovery project for those with alco-hol problems. He had been sober for five months when he was sent for an eval-uation of his cognitive abilities, such assessment forming part of the planningof his rehabilitation. ZS also stated to his doctor his concern that he was unin-telligent but his doctor did not consider this to be the case. He was highly moti-vated to attend for assessment and to do well. He saw it as a means of findingout whether he had any worthwhile abilities. He was also quite worried aboutthe possibility of brain damage after such a long period of alcohol abuse.

Tests of memory and new learning were carried out first.

The relative ease with which he handled the tasks sensitive to disorders ofnew learning (Logical Memory, Visual Reproduction and Associate Learning)was immediately reinforcing to ZS.

This performance was surprisingly unexpected in view of his good per-formances on the WMS, but it is not uncommon in such patients, where thepathological process or processes resulting from alcohol abuse often result indifficulty with complex learning especially where subjects must generatestrategies of learning and recall for themselves.

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WMS Form I

Information 5 Digits Total 10 (6,4)

Orientation 5 Visual Reproduction 11

Mental Control 6 Associate Learning 16 (6,1; 6,2; 6,4)

Memory Passages 9

MQ 114

RAVLT

List A List B List A List A

Trials 1 2 3 4 5 Recall Recall Recognition

Correct 5 7 7 9 9 6 8 13

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A short version of the WAIS-R was used to estimate current levels of func-tioning in a variety of areas and an estimate of probable premorbid abilitybased on subtests such as Information and Comprehension, which appearrelatively stable in the face of years of heavy drinking. It was thought that aftera long period of abstinence ZS’s intellectual functioning would be stable.

Apart from a non-specific slowing affecting the Digit–Symbol Substitutionsubtest there were no quantitative or qualitative features to suggest unsus-pected cognitive deficits.

Despite the apparent preservation of memory and intellectual abilities at alevel consonant with premorbid expectations, we have found that patients witha history such as that of ZS often have a serious problem with any degree of newlearning that involves benefiting from experience (see Ch. 4 and Walsh 1991).

ZS applied himself diligently to the task, insisting that he would get it righteventually. A stable, error-free performance might be expected in 15 trials or lessin someone of his estimated premorbid ability. His performance exemplifies veryclearly the problem of ‘error utilization’ or inability to perfect the learning of anovel, relatively complex procedure requiring integration over time. In this casethe single error on each of the last six trials was made at a different choice point.

This learning difficulty may easily escape notice unless appropriate tests areused. Such tests need to have the following characteristics: (i) novelty; (ii) com-plexity; (iii) self-direction; and (iv) integration over time.

We have found this imperfect learning disorder to correlate highly withsuccess or failure in job retraining and getting back into stable employment inindividuals such as ZS, and the prognosis in these cases should be guarded.Further examination usually reveals the presence of other indices of reductionin adaptive behaviour.

Hysterical pseudodementiaCASE: XW

This 60-year-old woman had worked as a technical assistant in a laboratoryuntil a few years before her present referral for possible dementia.

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WAIS-R Scaled Scores

Information 11 Digit Symbol 15

Comprehension 11 Block Design 9

Similarities 9 Object Assembly 10

Austin Maze (Milner Pathway)

Trial 1 2 3 4 5 6 7 8 9 10

Errors 22 30 15 14 11 10 12 6 7 5

Trial 11 12 13 14 15 16 17 18 19 20

Errors 5 5 5 4 5 6 4 5 5 4

Trial 21 22 23 24 25 26 27 28 29 30

Errors 2 1 3 3 4 2 1 1 1 1

Trial 31 32 33 34 35 36 37 38 39 40*

Errors 2 1 1 2 1 1 1 1 1 1

*Discontinued after 40 trials.

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The difficulties began in 1981 when she suddenly became unable to write andwhen seen in 1983 was unable to write even her own name. The onset of this dif-ficulty was not accompanied by any other signs of neurological deficit. Neithershe nor her husband reported any major medical or psychological problemsprior to this sudden onset. She did have a history of hypertension but this waswell controlled on medication. There had been no history of other neurologicalsymptoms apart from left-sided headaches particularly during times of stress.

Since the onset of her writing problems, XW reported that she had experi-enced increasing difficulties with her memory and in carrying out daily tasks.She reported rapid forgetting, being unable to remember where she put things,and hanging up the telephone and immediately forgetting the message or rea-son for the call. She stated that she was unable to remember day-to-day eventsor even what day it was. She was unable to cook a simple meal, do the shop-ping, handle money, knit or sew her own clothes, tasks she had previously per-formed with ease. Her husband reported that if his wife attempted any routinetasks she would just ‘dither’ and become upset. Consequently, he had takenover the majority of the domestic responsibilities.

XW described herself as a perfectionist. She stated that she found itextremely distressing, frustrating and even frightening when she found herselfunable to perform everyday tasks. Her degree of insight seemed surprising inview of the described severity of her complaint. During the assessment she waspleasantly cooperative but this was punctuated by periodic bouts of uncon-trolled weeping. After each of these she rapidly regained her composure andwas quite willing to carry on. Throughout the session she displayed apparentcomprehension and word finding difficulties.

The validity of what appears to be a very severe amnesic difficulty wascalled into question because the level of performance was out of keeping withher presentation during examination. Despite scoring zero on Orientation sheshowed clear evidence of recording ongoing events. While unable to give herdate of birth and other well-learned information she was able to recall thenames of current and former political figures with ease. Of the two prose pas-sages she produced only one piece of information and questioning producedno additions. Fragments of the three cards of Visual Reproduction producedanother score of zero (Fig. 10.9). Finally, unlike most patients with moderatedementia, she was unable to produce even a modest number of responses tothe ‘easy’ associations of the Paired Associate subtest.

It seemed to the examiner that this might reflect an attempt to enact the roleof ‘sicker than the sickest’ and a possible differential diagnosis of hystericalpseudodementia was entertained. This very simple examination took over anhour because of extreme slowness, complaints of not being able to understandthe simplest instructions, and time out for bouts of weeping.

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WMS Form I

Information 4 Digits Total 4 (4,0)

Orientation 0 Visual Reproduction 0

Mental Control 2 Associate Learning 4 (3,0; 3,0; 2,0)

Memory Passages 0.5

MQ 57

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Next an attempt was made at supraspan learning using only five digits.Despite ten trials, XW showed no evidence of even approximating the series.Testing was then abandoned.

During the second examination, despite the passage of four weeks withoutsignificant change, XW spontaneously recalled the examiner’s name. Whenasked to write her name and a simple sentence to dictation she produced asmall amount of illegible scrawl (Fig. 10.10).

To check the presence of a pseudoneurological memory disorder, XW wasgiven the 15-item ‘memory’ task of Rey cited in Lezak (1976, p. 476 f, 1983).‘The principle underlying it is that the patient who consciously or uncon-sciously wishes to appear impaired will fail at a task that all but the mostseverely brain – damaged or retarded patients will perform easily.’ Her perform-ance seemed consistent with a pseudodementia (Fig. 10.11).

Finally, XW’s reading was characterized not only by dysfluency but also bythe insertion of material that was not in the original text.

During this second visit further evidence came to hand of inconsistencies inher behaviour. For example, while she was unable to knit or cook a simple mealshe was quite able to drive herself into the country to visit friends.

Psychiatric opinion concurred with the diagnosis of hysterical pseudode-mentia and treatment was commenced. Neurological examination and CT scancarried out between the two testing sessions had been normal.

Keeping abreast of the times

The next case illustrates the integration of neuropsychology with other branchesof neuroscience and demonstrates how clinical neuropsychology can play a

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Fig. 10.9 Case XW. Recall of the three cards of the Wechsler Memory Scale, Form 1.

Fig. 10.10 Case XW. Writing to dictation. A, Attempts to write name; B, the sentence‘the cat ate the fish’.

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significant part in areas of complex clinical problem solving. It also highlights theneed for clinical neuropsychologists to keep abreast of the basic concepts ofthe disciplines with which they are in contact. The following case was providedby Professor Saling (Neuropsychology) of the Austin Hospital, Melbourne.CASE: PE

PE was seventeen years of age when she was referred for investigation andpossible surgical treatment of refractory partial seizures. A range of antiepilep-tic medications had been ineffective. Her early developmental history wasessentially uneventful. Pregnancy and delivery were normal, and there were noreports of any early febrile convulsions. Between the age of one and two years,her parents observed a brief episode during which she had trouble with walk-ing, but no professional advice was sought and the significance of this event isunclear. Her first seizure manifested as an episode of non-convulsive statuswhen she was four years of age. She was found stumbling around and crash-ing into walls. This automatism then evolved into generalized stiffening of thebody. She became apnoeic and was admitted to the intensive care unit forventilatory support and management of status epilepticus.

Though she lagged behind her peers at school in reading, spelling, andarithmetic she had no further attacks until the age of ten years, when she hada generalized tonic clonic seizure in her bed at night. These events becamemore frequent over the next few years, and were occurring once every twomonths by the time she was seventeen. After these events she was exhaustedand slightly confused for a while. These seizures were preceded by an aura,often by as much as a day. In cases such as this, the presence of an aura mightgive the first clues about the region of the brain from which the seizures areemanating. In this case the aura consisted of some general features, such asdizziness and nausea, which do not have any clear localising significance. Theyalso consisted of auditory phenomena in the form of voices she could notunderstand. As is sometimes the case in epilepsies that originate in neocorticalstructures, which are richly interconnected with one another and thereforeallow for the spread of epileptiform discharges along a variety of pathways,she suffered from more than one seizure type. She also had absence-likeseizures consisting of staring, head nodding, and stereotyped verbalizationsuch as, ‘yes, yes, yes’. These too were preceded by an aura of ‘jumbled voices’.These seizures would end suddenly, and she could continue with whatever she

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Fig. 10.11 Case XW. Response to Rey’s 15-item memory test.

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was doing before the seizure started. The significance of the third type of eventwas uncertain, but these were thought to be simple partial seizures consistingof a sudden onset of left-sided headache, with no alteration in awareness. It isof localizing interest that the auras did not involve visual, gustatory, or olfac-tory hallucinations.

The semiology of her seizures was better defined on video-monitoring. Thegeneralized tonic clonic events were in fact preceded by a brief period of oralautomatisms, deviation of gaze to the right, raising of the right arm, and unin-telligible vocalization. A generalized tonic clonic phase then followed. Thissequence of events, namely, local automatisms and unilateral movements fol-lowed by generalized (bilaterally symmetrical) movements, defines herseizures as focal in origin but then spreading to involve both hemispheres.Some of the early behavioural manifestations of her major seizure type areright sided (gaze deviation, arm raising), and taken together with the jumbledverbal content of the aura raise the question of a left temporo-parietal focus.Electrographically, there were frequent abnormal discharges in periodsbetween overt convulsions that suggested a left fronto-temporal origin, spread-ing to the other side of the brain.

Magnetic resonance imaging of the brain revealed an area of hyperintensityinvolving the left parietal cortex and underlying white matter in the region ofthe supramarginal gyrus. This was associated with a loss of distinctionbetween grey and white matter in the region, i.e. blurring of the grey–whitejunction (Fig. 10.12). While other pathologies could not be excluded defini-tively, the MRI appearance suggested focal cortical dysplasia. There were noother abnormalities and, in particular, the hippocampal volumes were normal.Resting cerebral glucose uptake on FDG-PET showed a well-defined metabolicdefect in the left posterior parietal lobe, corresponding with the region of MRhyperintensity, with an extension into the posterior aspect of the superior tem-poral gyrus. In focal epilepsies the functional abnormality is often more widelydistributed than the structural abnormality, and in this case there was reducedmetabolism in the mesial and anterior portions of the temporal lobes, the leftmesial temporal region being more affected than the right. Single photon emis-sion computed tomography (SPECT) showed a discrete area of reduced bloodflow (hypoperfusion) in the left posterior parietal region on interictal study,that is, during the absence of any seizure activity. This is further evidence thatneurobiological function is reduced at the site of the structural lesion. Duringan overt seizure the SPECT study showed a relative increase in blood flow inthe previously hypoperfused region. This finding strengthens the hypothesisthat her seizures begin in the left posterior parietal cortex since it is well estab-lished that seizure activity is associated with increased blood flow in the regionfrom which it originates.

Anatomically, the lesion lies in cortex usually associated with language andother symbolic functions. The auditory content of the aura heightens the likeli-hood that the seizure focus involves cortex that is actively mediating languagefunction. For this reason, careful consideration needs to be given to theneurocognitive risks of resecting the lesion. The principles of preoperativeneuropsychological evaluation are reasonably well established in temporal lobeepilepsies. Extratemporal epilepsies are highly variable in terms of the locationof the lesion, and demand an individualized and hypothesis-driven approach.

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Neuropsychology. The key neuropsychological goal in this case was toassess the risk of a postoperative aphasia, and to assist in ensuring a good lan-guage outcome. The lateralization and intracerebral localization of language isfundamental to the neuropsychological decision making in this case. PE is lefthanded and she has a family history of left handedness, which raises the like-lihood of anomalous representation of language. Early lesions in or aroundputative language cortex might also influence the pattern of language repre-sentation, but whether or not they are consistently associated with interhemi-spheric shifts in language is controversial in the case of focal dysplasias. Thecontent of her auras and ictal vocalization suggests that the left-sided seizurefocus is interfering with language mechanisms. Her learning difficulties affectfunctions that are dependent, at least in part, on the left inferior parietal lobule,and this too might suggest (although rather weakly) that the epileptogeniclesion has interfered with the development of cognitive functions associatedwith that region.

At this point in the preoperative evaluation, a problem-oriented neuropsy-chological study is an important guide to planning the surgical resection in theinterest of avoiding or minimizing postoperative cognitive impairment. Thelogic of the neuropsychological approach in cases like this is determined by therather special nature of developmental lesions and the relationship between thelesion and the epileptogenic zone. Although dysplastic lesions are physiologi-cally active, it is doubtful if a dysplastic region is able to mediate coherent cog-nitive activity. Rather, lesions of this type change the way in which functionsare represented, often displacing them to adjacent regions. The epileptic zoneis not necessarily restricted to the lesion, but might extend into adjacent andgrossly normal tissue. Resection of the anatomical lesion itself poses a lower(but not necessarily negligible) risk to cognition, but might not effect an opti-mal seizure outcome. A wider resection might improve the seizure outcome butmight produce unacceptable cognitive complications. The neuropsychologist

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Fig. 10.12 Case PE. Coronal scans of the brain through the parietal region. The leftimage displays a resting PET scan, which shows regional cerebral glucose uptake(blue = low uptake; yellow–red = high uptake). A region of low uptake is evident inthe left parietal lobe. The right image displays a magnetic resonance image, showing aregion of thickened (dysplastic) cortex in the left parietal lobe corresponding with themetabolic defect. Note: For those unfamiliar with imaging please note that suchdepictions are shown as if the brain were facing the reader, i.e. the left side of thebrain is to the right of the picture and vice versa.

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needs to understand the interictal effects of the lesion on cognition (if any), aswell as the distribution of cognitive function in adjacent cortex. This end is bestachieved by synthesizing the results of behavioural study, functional neuro-imaging, and electrical mapping.

PE is of average intelligence, as the following WAIS-R age-scaled scoressuggest.

Her performance on the Information and Arithmetic subtests are not quitein keeping with the other scores, and might reflect her longstanding learningdifficulties.

Performance on the Wide Range Achievement Test (WRAT-3) revealed a sig-nificant lag (in terms of grade scores) in the acquisition of basic scholastic skills:

Against the background of average intelligence, the WRAT-3 findings sug-gest the presence of specific learning disabilities.

As one might expect in the case of developmental neuropathology, the lesiondid not result in a classical focal left parietal syndrome: ideomotor praxis, fin-ger gnosis, left–right orientation, naming, sentence repetition, and appreciationof logico-grammatical relationships were intact. It was also clear from her BlockDesign performance and her competent copy of the Complex Figure of Rey thatthere was no constructional disorder. However, the above findings cast a ques-tion mark over her ability to calculate, and the possibility of a frank dyscalculiawas pursued. On specific examination basic arithmetic operations were intact.In particular she was able to subtract, for example, 35 from 86 correctly.However, she made consistent errors in subtracting, for example, 19 from 23.This difficulty has the form of a spatial dyscalculia, and while it might simplyrepresent the failure to acquire a specific arithmetic subskill, it lends someweight to the view that resection of the lesion is not without the risk of post-operative cognitive loss.

Consistent with the structural integrity of the left and right mesial temporalregions, verbal paired associate learning and recall of the Complex Figure ofRey were normal:

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Information 7 Picture Completion 9

Arithmetic 6 Block Design 11

Digit Span 11 Digit-Symbol 10

Similarities 9

Vocabulary 9

Reading 2.7

Spelling 1.9

Mathematics 2.6

PAL 3/2, 6/4, 6/4

RCFT recall 25/36

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While an interictal dysphasia would have strengthened the case for left-lateralization of language, such findings are rare in dysplastic lesions, even whenthe lesion involves classical language cortex. A functional magnetic resonancelanguage study, using a noun–verb generation paradigm, showed a task-relatedresponse in the left inferior frontal cortex as well as left-sided posterior activationadjacent to the lesion. This finding indicated that epilepsy surgery in posteriorperi- and retro-Sylvian cortex could pose a risk to language and related cognitivefunctions, and careful tailoring of the resection would be necessary. This in turnprovided a rationale for the implantation of intracerebral electrodes.

A strip of intracranial electrodes was implanted over the surface of the tem-poral and parietal lobes, for the purpose of mapping the epileptogenic zone andlanguage. Focal electrical stimulation interferes with, or ‘switches off’ thestimulated region of cortex. If that piece of tissue is mediating language, aphasicerrors or language arrest should be detected. During stimulation naming,repetition, and high-level comprehension were examined. Stimulation withinthe lesion failed to produce any language abnormalities. However, stimulationin the immediately adjacent posterior temporal region disrupted naming andsentence repetition. The resection was tailored to avoid this region, but includedthe supramarginal and angular gyri. Postoperative histopathology was consis-tent with cortical dysplasia.

Postoperatively language function was well preserved. A senior neuropsy-chologist noted that: ‘The surgery has not been accompanied by any discerniblealteration in her memory, language, or associated functions . . . we are opti-mistic that the surgery will be successful in alleviating [her] seizures’.

An open verdict

CASE: IJ

This 64-year-old motor mechanic was admitted after experiencing severalepisodes of recurrent ‘surges’ of sensation, which commenced in the legs, pro-gressed rapidly up the trunk and reached a climax in the head. The sensoryexperience was accompanied by unusual smells. The episodes typically lastedfrom 30 to 60 seconds and were followed by a brief period of confusion butthere was no loss of consciousness. His memory was defective for some timeafter the events but returned to normal a few hours later. There were no abnor-mal movements, auditory or visual hallucinations or feelings of derealizationor depersonalization. He had never been incontinent. There was no clear pre-cipitating event and he had sometimes had attacks while driving. The attackshad begun one year before but had become more frequent in recent times. Hismedications had included aspirin and trifluoperazine.

During the two days prior to admission he had had seven attacks. He volun-teered the information that his memory had deteriorated over the past two years,having to rely constantly on his notebook, and it is possible that the memory dif-ficulty pre-dated the onset of the sensory episodes. Over the past year he admit-ted to an examining psychiatrist that he was disturbed by certain recurringthoughts but there were no details as he requested them not to be recorded.

At the time of neuropsychological examination the reason for the attacksremained unclear. Differential diagnosis had included: transient ischaemic

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attacks; temporal-lobe epilepsy; psychosis; and early dementia. Clinical exam-inations made the diagnosis of transient ischaemia or psychosis most unlikelyand neuropsychological assessment was sought as an aid to diagnosis.

It was evident from his account of his past history that his remote memorywas intact and a screening of his immediate and recent memory was made.

Despite a good immediate memory, IJ did poorly on the three tests of newlearning (Logical Memory, Visual Reproduction, Associate Learning). Herecalled little of either memory passage and was unable to recall any morewhen asked specific questions. The pattern of performance was stronglysuggestive of a general amnesic disorder.

As one of the possibilities raised was an early dementing process, it was nec-essary to find out if his memory disorder was accompanied by other signs ofintellectual decline. The WAIS was administered over two sessions and thehigh level and quality of his performances overall threw the poor memory per-formance into sharp contrast. Dementia was now excluded.

Further evidence of IJ’s memory problem was revealed by the complex fig-ure of Rey. His copy was well planned and executed with a maximum score of36, while the recall at three minutes was rudimentary (Fig. 10.13).

A CT scan following this assessment revealed no abnormalities. EEG scalprecordings showed normal alpha activity present bilaterally. There was bilateralexcess of theta components, which was considered to be more marked on theleft but there was no clear lateralization. At this stage a diagnosis of temporal-lobe epilepsy was made and the patient was commenced on carbamazepine.

The relationship of what appears to be a clear cut and quite severe generalamnesic syndrome and temporal-lobe epilepsy remains unclear. Certainly in alarge number of younger cases we have not seen instances of an axial amnesia,though material-specific deficits are not uncommon. IJ’s epilepsy may have hada more sinister cause but he has not presented again at our hospital in the ensu-ing years. As is not infrequently the case, an open verdict must be entered.

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WMS Form I

Information 4 Digits Total 11 (7,4)

Orientation 4 Visual Reproduction 6

Mental Control 7 Associate Learning 6 (1,0; 5,0; 6,0)

Memory Passages 4

MQ 89

WAIS Scaled Scores

Information 13 Picture Completion 12

Arithmetic 15 Picture Arrangement 11

Comprehension 16 Block Design 12

Similarities 12 Object Assembly 10

Digit Symbol 10

VIQ prorated 128 PIQ 123

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CASE: QT

This 45-year-old bank manager was admitted to hospital following a suicideattempt involving motor vehicle exhaust fumes. He was confused and disori-ented for four days and his first clear memories were of a family visit five daysafter admission, though he subsequently recalled isolated events from the thirdand fourth days. He was amnesic for the incident but recalled setting out in hiscar. EEG and CT scan on the third day were both normal. The reason for hisattempt remained unclear but may have been related to difficulties with hissecond marriage.

On examination on the sixth day he was pleasantly cooperative and seem-ingly unconcerned with the fact that he had tried to commit suicide. He com-plained of a severe memory difficulty.

As amnesic deficit looms large in many cases of carbon monoxide poison-ing, testing commenced with the Wechsler Memory Scale Form I.

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Fig. 10.13 Case IJ. Recall of Rey Figure at three minutes.

Similarities 11 Block Design 12

Digit Span 12 Object Assembly 8

WMS Form I

Information 5 Digits Total 14 (7,7)

Orientation 5 Visual Reproduction 12

Mental Control 7 Associate Learning 8 (2,0; 4,2; 6,0)

Memory Passages 7

MQ 103

Arithmetic 14 Picture Completion 10

Digit-Symbol 12 Picture Arrangement 12

WMS Form I

Memory Passages 6

Visual Reproduction 14

Associate Learning (6,0; 6,1; 6,2) 12

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QT had particular difficulty with new verbal learning. We have found the ‘dif-ficult’ items on Paired Associate learning particularly sensitive in these cases.However, we have usually found a general amnesia in previous instances of carbonmonoxide poisoning so that the good performance on Visual Reproduction wasunexpected, though we have seen such a sparing in cases of alcohol-related amne-sia, which have all the features of Korsakoff psychosis (see Ch. 2, and Walsh 1991).

The RAVLT performance was marked by virtually no extension beyond hisimmediate memory span (7), a marked interference effect, and poor recognitionmemory.

Copy of the complex figure of Rey was complete and well organized, butonly the main outline was recalled at three minutes (score 10/36).

Finally, four subtests of the WAIS-R showed a relatively poor performanceon only Object Assembly.

Testing was terminated due to lack of time, with the impression of anamnesic disorder largely uncomplicated by more widespread intellectualloss. Prognosis was reserved as we have seen varying degrees of recoveryin amnesic disorders following carbon monoxide poisoning and hypoxic events.

A second neuropsychological assessment was done at one month. With oneexception, the repeated testing, WMS (Form II), RAVLT and Rey Figure, pro-duced almost identical results. There was still a discrepancy between a goodperformance on Visual Reproduction and measures of verbal learning. Thisdissociation was confirmed by the BVRT given with a 15 second delay. QT hadno difficulty; eight of ten correct with only two errors. The clear differencenoted was on the RAVLT. While the poor acquisition and interference effectwere identical to the early examination, the Recognition score had risen fromseven to thirteen of a possible fifteen.

Other subtests of the WAIS-R produced a level of performance as before.

A third examination was made at three months. The patient said hismemory was still poor but had improved somewhat as he was now able torecall some telephone numbers and addresses. Testing was restricted to mem-ory as there had been no indication of other cognitive deficits. In keeping withhis subjective report there were slight gains over the two month period thougha sizeable memory deficit still remained.

The great difficulty with spontaneous recall and the marked interferenceeffect remained as serious as before and the prognosis began to look gloomy. In

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RAVLT

List A List B List A List A

Trials 1 2 3 4 5 Recall Recall Recognition

Correct 6 5 7 8 8 6 3 7

Similarities 11 Block Design 12

Digit Span 12 Object Assembly 8

Arithmetic 14 Picture Completion 10

Digit-Symbol 12 Picture Arrangement 12

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an endeavour to see whether logical structure of the material to be learnedinfluenced learning and retention, two of the tests of Lhermitte and Signoret(1972) were given (see Walsh 1991). The test of Spatial Arrangement was mas-tered in four trials, a normal performance, and an even better performance ofonly two trials to criterion on the test of Logical Arrangement suggested thatmemory retraining might be advantageous in this case since there was reasonto believe that visual memory was relatively spared and the ability to benefitfrom logical structure to aid learning was clearly present. Follow-up wassuggested but the patient failed to keep the next appointment.CASE: YQ

Education: Post graduate diplomaOccupation: Property management consultantFollowing the death of his wife a few years before, this successful 60-year-old

businessman had taken up parachuting. Several of his jumps were not well exe-cuted and on one of them he was badly shaken though apparently not unconscious.

Following this incident (28 December 1983), YQ developed severe left-sidedheadaches, drowsiness, vomiting, poor concentration and photophobia.During the next two weeks, however, he continued his parachute jumpingdespite persistent headaches and concentration difficulties. He was involved inthree minor car accidents on 2 January 1984. On 3 January 1984 he eventuallysought medical attention, and was admitted to hospital where CT scanrevealed a subdural haematoma. At operation a mixture of old and fresh bloodwas evacuated from the left fronto-temporal region.

Postoperatively there was motor aphasia and mild right-arm weakness butthese were almost normal on discharge two weeks later.

At neuropsychological assessment at two months, YQ was cooperativealthough somewhat flippant and facetious. He said that his memory, whichwas poor for some weeks, had returned to normal but he still had mild word-finding difficulties when tired.

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WMS Form I

Memory Passages 6

Visual Reproduction 14

Associate Learning 12 (6,0; 6,1; 6,2)

RAVLT

List A List B List A List A

Trials 1 2 3 4 5 Recall Recall Recognition

Correct 4 7 8 9 9 5 1 3

WMS Form I

Information 6 Digits Total 13 (8,5)

Orientation 5 Visual Reproduction 12

Mental Control 7 Associate Learning 8.5 (4,0; 5,1; 6,0)

Memory Passages 13

MQ 122

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The principal finding of marked difficulty with the ‘hard’ pairs of AssociateLearning was further investigated with the RAVLT.

This test highlighted a verbal learning difficulty of some severity. Apartfrom the very low level of acquisition, the unsystematic order of recall oversuccessive trials suggested a ‘frontal amnesia’ (see Ch. 4).

Because of this deficit and the known location of the lesion, the ensuingassessment included several tests often found sensitive to frontal lobe dys-function together with several subtests of the WAIS-R.

Apart from a generalized slowing on all tests which robbed him of timecredits, YQ showed a concept level on the Similarities subtest lower thanexpected for his educational and occupational background.

Verbal fluency test 1. The result (F-11; A-10; S-12) was well below expecta-tion and thought to be consistent with residual dysfunction in the left frontalregion.

Complex figure of Rey. Copy: score 34/36 but poorly organized. Recall: score19/36. A considerable reduction in keeping with the provisional diagnosis offrontal amnesia.

YQ’s performance strongly supported the hypothesis of residual frontal-lobe dysfunction. After making only four errors on trial seven, a person of hispremorbid competence should have reached a stable error-free performance inthe next few trials yet it took him more than 25 further trials to reduce his errorsto zero and there is no guarantee in such a case that he would be able to main-tain this error-free condition. The difficulty demonstrates very clearly what inChapter 4 was termed the problem of error utilization.

Advice was given on the possible disruptive effects of his brain injury on hiswork performance.

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RAVLT

List A List B List A List A

Trials 1 2 3 4 5 Recall Recall Recognition

Correct 5 5 7 7 7 5 3 12

WAIS-R Scaled Scores

Information 14 Block Design 10

Similarities 10 Object Assembly 10

Digit Symbol 8

Austin Maze (Milner Pathway)

Trial 1 2 3 4 5 6 7 8 9 10 11 12

Errors 26 21 7 12 6 6 4 5 7 5 5 2

Trial 13 14 15 16 17 18 19 20 21 22 23 24

Errors 3 3 1 1 2 4 1 2 3 2 1 1

Trial 25 26 27 28 29 30 31 32 33 34

Errors 1 1 1 2 2 1 1 1 0 0

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A second assessment was made at eight months. YQ had returned to his for-mer position as national manager of a major corporation. He described a num-ber of personality changes, which he dated to the time of his injury. Hedescribed himself as more ‘laid back’ at work and less committed, preferring todelegate work. He reported being more forthright and outspoken than before.Apart from some minor difficulty recalling names he reported no significantmemory problems. His minor word-finding difficulty persisted.

To check any recovery of cognitive functioning parallel forms of tests previ-ously used were employed where possible.

WMS – Form II. Despite a rise in MQ from 122 to 132 due to small improve-ments on several subtests, YQ still showed no facility in learning the new ordifficult pairs of the Associate Learning subtest. Score 11 (6,0; 6,1; 6,1). Therewas a modest gain on the RAVLT, but this was still considerably below par fora man of his premorbid ability.

Complex figure of Rey. The copy score was again 34, but the organizationpoor. The recall score was even less than before and showed several featuresdescribed with frontal lobe lesions (see Messerli et al 1979). YQ could not resistthe impulse to draw a house (possibly aroused by the figure), which he thenscribbled out (Fig. 10.14).

Verbal fluency had increased only marginally from a mean of 11 to a meanof 12.3.

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RAVLT

List A List B List A List A

Trials 1 2 3 4 5 Recall Recall Recognition

Correct 5 7 7 10 11 5 9 151

Fig. 10.14 Case YQ. Frontal dysfunction in recall of Rey Figure.

Austin Maze (Milner Pathway)

Trial 1 2 3 4 5 6 7 8 9 10 11

Errors 37 18 15 14 9 13 10 4 4 4 7

Trial 12 13 14 15 16 17 18 19 20 21 22

Errors 7 3 3 1 2 5 3 1 1 0 0

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Once again while there might be some improvement, there was still a sig-nificant problem of error utilization some considerable time after injury. It alsobecame clear at this second examination that YQ had little or no insight into thenature and extent of his deficits.

Postscript. At neurosurgical review two months later, YQ expressed a strongdesire to retire from work as he felt that he was not able to perform intellectuallyas well as he had prior to his accident. His superior obviously aware of the sub-tle but pervasive changes wrought by the frontal injury supported the suggestionof immediate retirement. The patient was still keen, however, to continue hisparachute jumping. One can only surmise why he took this on in the first place.CASE: QS

This 56-year-old male right-handed, formerly high-functioning, general practi-tioner was referred with a presumptive diagnosis of Alzheimer’s disease afterexperiencing more than a year of slowly progressing vocational difficulties.

Initial symptoms were regarded as memory difficulties. He reported beingsurprised that commonly used drug names no longer meant anything to him.When required to re-prescribe medications, he found he no longer recognizedmany specific drugs. Occasionally he would ask patients the indications for thesemedications, and when told, found such prompts did not cue any additionalfamiliarity. He created notes on medical topics and specific drugs to aid him.Patients began to complain that he seemed ‘confused’ and hesitant at times.

His wife noticed difficulties at least two years previously. Whilst overseas,he seemed less able to cope with the busy schedule, becoming withdrawn, eas-ily frustrated and reserved. He was found spending more time reading profes-sional material than formerly. He had been an eloquent orator, but a recentwedding speech was regarded as uncustomarily simple, and he had found itdifficult to spell or construct words during games of Scrabble. His wife alsocommented that his powers of logic seemed affected, though his personalitywas similar and temporal orientation and knowledge of current affairs werepreserved. Personal hygiene, grooming, driving and social independenceremained normal. No unusual medical symptoms were present.

There was no other past, family or social history of note. He had neversmoked and at most drank a single glass of whisky or wine each day.

He was initially referred to a neurologist, who reported no elementary neu-rological or general abnormalities, and then referred him to a psychiatrist. Henoted no formal psychiatric or mood disorder, but found prominent languagedifficulties particularly with word selection, recall and usage, together withslow speed of information processing, organizational and abstraction impair-ments, and difficulty encoding and recalling verbal information with impover-ished recall of complex visual information. The psychiatrist felt that suchwidespread deficits made Alzheimer’s disease the most likely diagnosis, andfelt that neuroimaging was not necessary. He was referred to our unit for neu-ropsychological screening prior to experimental drug trials.

Neuropsychological examination. He was alert, cooperative, well-groomed,polite, appropriate in affect and, although correcting himself repeatedly, wasoriented to time and location, and knew political figures and current events.His initial verbal responses were frequently incorrect though within the correctsemantic category. He would then show frustration and attempt to correct hisanswer, usually only ceasing when correct. Hesitations and word-finding

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problems dominated his performances. Premorbid verbal intelligence was pre-dicted to be in the superior range (New Adult Reading Test seven errors,predicted Verbal IQ 122, Nelson & O’Connell 1978).

He could repeat five digits forwards and four backwards. Routine mentaloperations were performed more poorly than expected, e.g. counting fromtwenty to one in 31 seconds, reciting months of the year forwards in four secondsbut backwards in 73 seconds, and during serial addition of three hesitated, for-got current numbers and made repetitions. He appeared to have difficulty main-taining task instructions as well as current items in mind simultaneously.

Language tasks were particularly impaired. Spontaneous language wasfluent, grammatical and adequate for conversational expression, though withoccasional semantic paraphasias. Repetition was preserved. Confrontationnaming was severely impaired. He was only able to name correctly the highestfrequency items of the Boston Naming Test, and was not assisted by semanticor phonemic cues. He could not correctly complete the sentence: ‘a tool totighten a nut on a bolt is a . . .’. Definitions of telescope, barometer andperiscope were slow and laborious. Comprehension was intact for passive andrelational constructions, names of fingers and sides of the body and writing,although slow, was correct. Mental arithmetic was very poor, e.g. 6 + 5 is ‘. . .11’, 13 − 7 is ‘. . . don’t know’, 20 − 7 is ‘. . . 13’, 17 × 3 is ‘. . . don’t know’.

Verbal fluency was markedly impaired, particularly for semantic categories,e.g. animals 2, vegetables 2, supermarket items 4. For animals, he stated ‘par-rot, dog . . .’ and then could not think of any others for the entire minute. Hisperformance for word generation using initial letters was poor (F-7, A-5, S-8).He could recall the route home correctly in terms of direction of consecutiveturns, but not all the names of the important streets along the way.

He was not able to improve his recall of the 15 words of the RAVLT signifi-cantly beyond his verbal span, showing little attempt at organizing his recall orsuccess in the middle words of the list. When attempting to listen to the words,he commented ‘they disappear . . . go straight through’. Retroactive interfer-ence was prominent, and recognition relatively better, though with multipleintrusions.

His copy of the Rey–Osterreith Complex Figure was poorly organized (score30/36, 20th percentile) and recall markedly impoverished (score 9/36, <10thpercentile).

Simpler measures of encoding and recall, e.g. the Three Words Three ShapesTest (see Lezak 1995) and memory for three objects in three locations, were moreeasily encoded but he showed greater difficulty recalling verbal than visual mate-rial after interpolated tasks. Multiple choice presentation did not improve hisrecall noticeably for verbal items. On the other hand, visual material was recalledaccurately even two hours later, suggesting that language difficulties may under-lie these many failures, rather than a general amnesic syndrome.

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RAVLT

List A List B List A List A

Trials 1 2 3 4 5 Recall Recall Recognition

Correct 3 5 5 6 7 3 3 12 (+6)

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Simple visuoconstructive tasks were performed well, and he was able to pointout multiple hidden figures in an embedded figures test, but more complex taskstended to be poorly organized and executed. Other executive deficits were alsopresent, suggesting that visuospatial impairments were secondary to executivenot visuoperceptive difficulties. On part B of the Trail Making Test he reverted toconnecting consecutive letters. He could not correctly perform conflicting motortasks with both hands, or reproduce simple hand positions without verbal assis-tance. He could not complete the Milner Pathway of the Austin Maze.

Although he indicated understanding of the task and approached it in a log-ical manner, he quickly forgot the location of central choice points, making boththe same and new errors repeatedly, and became too frustrated to continue. Inaddition, although he evinced frustration with some of his performances, heappeared less concerned than expected.

Discussion. On the basis of these performances, it was clear that he was per-forming well below expectation. The history of insidious onset, gradual progres-sion, early and disproportionate difficulties with language-based tasks suggestedan intrinsic brain disease asymmetrically affecting his dominant hemisphere. Hislanguage deficits resembled a transcortical sensory aphasia with very severesemantic difficulties suggesting a left posterior or inferior temporal region lesion.His initial difficulties recalling medical terms resembled ‘alienation du mot’(estrangement of word meaning, see Poeck & Luzzatti 1988). Executive deficitswere mild but suggested added anterior involvement. Relatively spared func-tions included phonology, syntax, syntactic comprehension, autobiographicaland episodic memory, visuospatial abilities and non-verbal memory.

A similar clinical pattern has been reported within the spectrum of primaryprogressive aphasia (Basso et al 1988, Weintraub et al 1990, Weintraub &Mesulam 1993, Kertesz 1997, Mesulam et al 1997). Others have separately clas-sified the grammatically fluent form as ‘semantic dementia’ (Snowden et al1989, Hodges et al 1992, Talbot et al 1995) emphasizing the dissolution ofsemantic information stores including the lexicon, but relative preservation ofother cognitive abilities. Specific asymmetrical left inferior temporal neocorti-cal atrophy is a reported feature of semantic dementia (Chawluk et al 1986,Hodges et al 1992, Mesulam et al 1997), so neuroimaging studies were recom-mended.

MRI showed predominant inferolateral left temporal lobe atrophy. Positronemission tomography confirmed asymmetrical hypometabolism of both tem-poral lobes extending into the left frontal cortex. The hypometabolismappeared to spare the superior and middle temporal gyri making it atypical forAlzheimer’s disease. These findings accorded well with those reported insemantic dementia, as well as the patient’s clinical features.

It is important to differentiate this condition from Alzheimer’s disease. Thepathology underlying semantic dementia is variable, and may include non-specific superficial neuronal loss, gliosis and spongiform degeneration or

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Austin Maze (Milner Pathway)

Trial 1 2 3 4 5 6 7 8 9 10 11 12 13*

Errors 14 7 9 7 6 6 4 3 4 7 2 1 3

*Client gave up after 13 trials.

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Alzheimer’s disease (Weintraub & Mesulam 1993, see Neary 1997). Inclusion ofsuch patients in trials of Alzheimer’s disease-related medications may con-found results. Patients with semantic dementia tend to present around the ageof 55 years, resembling more the epidemiological spectrum seen with fronto-temporal dementia (see Ch. 3), and there may be similar genetic implications.Prognosis may also be different with some patients showing several years ofrelative stability and preserved non-language functions making their qualityof life dramatically better than modal Alzheimer’s-disease patients. Theprogression of deficits is different with a longer course on average for thenon-Alzheimer’s-disease patient. Counselling should take this into account,particularly the prospect of progressive language dissolution out of proportionto other intellectual deficits, or the development of additional executiveimpairment.

Course. Over the next two years, QS continued to deteriorate cognitively.His lexical knowledge dramatically deteriorated with simplification of his con-versational speech, frequent hesitations and word-finding pauses, and confu-sion of simple medical terms, e.g. using ‘sphygmomanometer’ for stethoscopeand denying any knowledge of the word ‘cystitis’ or specific antibiotics. Pastacquaintances were forgotten completely, including the associations of old pho-tographs, to which he started adding subtitles. Spelling deteriorated markedly,so that he tended to write with letters poorly differentiated. He became con-fused in conversations involving several people. His insight further deterio-rated, as did his awareness of social mores. His wife could no longer take himto live concerts since he was apt to be noisy or talk abruptly without the usualregard for the rules of social intercourse. He became more rigid in his manner,more impulsive and short-tempered. He once became angry with their petlabrador, and threw him bodily out of the back door. At times he was child-like,following his wife around. He remains physically active but is continuingto deteriorate.

References

Basso A, Capitani E, Laiacona M 1988 Progressive language impairment without dementia: acase with isolated category specific semantic defect. Journal of Neurology, Neurosurgery,and Psychiatry 51: 1201–1207

Benjamin L T, Baker D B 2000 The Boulder Conference. American Psychologist 55: 233–254Binder L, Pankratz L 1987 Neuropsychological evidence of a fictitious memory complaint.

Journal of Clinical and Experimental Neuropsychology 9: 167–171Chawluk J B, Mesulam M-M, Hurtig H, Kushner M, Weintraub S, Saykin A, Rubin N, Alavi

A, Reivich M 1986 Slowly progressive aphasia without generalized dementia: studieswith positron emission tomography. Annals of Neurology 19: 68–74

Elithorn A 1965 Psychological tests. An objective approach to the problem of task difficulty.Acta Neurologica Scandanavica, Suppl. 13, Part 2: 661–667

Franzen M D, Burgess E J, Smith-Seemiller L 1997 Methods of estimating premorbidfunctioning. Archives of Clinical Neuropsychology 44: 367–373

Goldberg E, Costa L D 1986 Qualitative indices in neuropsychological assessment. In: GrantI, Adams K M (Eds) Neuropsychological assessment of neuropsychiatric disorders.Oxford University Pres, New York, pp. 48–64

Hampton J R, Harrison M J G, Mitchell J R A, Pritchard J S, Seymour C. 1975 Relativecontributions of history taking, physical examination, and laboratory investigation todiagnosis and management of medical out-patients. British Medical Journal ii: 486–489.

10N

euro

psych

olo

gical assessm

ent

447

Ch10.qxd 20/7/04 8:12 PM Page 447

Hodges J R, Patterson K, Oxbury S, Funnell E 1992 Semantic dementia: progressive fluentaphasia with temporal lobe atrophy. Brain 115: 1783–1806

Kaplan E 1988 A process approach to neuro-psychological assessment. In: Boll T, Bryant B K(Eds) Clinical neuropsychology and brain function: research, measurement and practice.American Psychological Association, Washington, pp. 129–167

Kaplan E, Fein D, Morris R, Delis D 1991 WAIS-R NI Manual. Psychological Corporation,San Antonio

Kertesz A 1997 Frontotemporal dementia, Pick disease, and corticobasal degeneration: oneentity or 3? 1. Archives of Neurology 54: 1427–1429

Kinsbourne M 1971 Cognitive deficit: experimental analysis. In: McGaugh J L (Ed.)Psychobiology. Academic Press, New York, Ch. 7

Kinsbourne M 1972 Contrasting patterns of memory span decrement in ageing and aphasia.Journal of Neurology, Neurosurgery, and Psychiatry 35: 192–195

Levin H S, Eisenberg H M, Benton A L (Eds) 1989 Mild head injury. Oxford University Press,New York

Lezak M D 1976 Neuropsychological assessment. Oxford University Press, New YorkLezak M D 1980 An individualized approach to neuropsychological assessment.

(Unpublished manuscript)Lezak M D 1983 Neuropsychological assessment, 2nd edn. Oxford University Press,

New YorkLezak M D 1988. IQ: R I P. Journal of Clinical and Experimental Neuropsychology 10:

351–361Lezak M D 1995 Neuropsychological assessment, 3rd edn. New York, Oxford University PressLhermitte F, Signoret J-L 1972 Analyse neuropsychologique et différenciation des syndromes

amnésiques. Revue Neurologique 126: 161–178Luria A R, Tsvetkova L D 1964 The programming of constructive activity in local brain

injuries. Neuropsychologia 2: 95–108Meehl P E 1954 Clinical versus statistical prediction. University of Minnesota Press,

MinneapolisMesserli P, Seron X, Tissot P 1979 Quelques aspects de la programmation dans le syndrome

frontal. Archives Suisses de Neurologie, Neurochirurgie et de Psychiatrie 125: 23–35Mesulam M-M, Johnson N, Grujic Z, Weintraub S 1997 Apolipoprotein E genotypes in

primary progressive aphasia. Neurology 49: 51–55Miller E 1983 A note on the interpretation of data derived from neuropsychological tests.

Cortex 19: 131–132Mortensen E L, Gade A, Reinisch J M 1991 ‘Best Performance Method’ in clinical

neuropsychology. Journal of Clinical and Experimental Neuropsychology 13: 361–371Neary D 1997 Frontotemporal degeneration, Pick disease, and corticobasal degeneration:

one entity or 3? 3. Archives of Neurology 54: 1425–1427Nelson H E 1982 The national adult reading test (NART): test manual. Windsor, Berkshire,

UK: NEFR-NelsonNelson H E, O’Connell A 1978 Dementia: the estimation of premorbid intelligence levels

using the new adult reading test. Cortex 14: 234–244Pankratz L 1979 Symptom validity testing and symptom retraining: procedures for the

assessment and treatment of functional sensory deficits. Journal of Consulting andClinical Psychology 47: 409–410

Pankratz L 1983 A new technique for the assessment and modification of feigned memorydeficit. Perceptual and Motor Skills 57: 367–372

Pankratz L, Paar G H 1988 A test of symptom validity in assessing functional symptoms.Zeitschrift für Klinische Psychologie, Psychopathologie und Psychotherapie 36: 130–137

Pankratz L, Fausti S A, Peed S 1975 A forced choice technique to evaluate deafness in thehysterical or malingering patient. Journal of Consulting and Clinical Psychology 43:421–422

Pankratz L, Binder L M, Wilcox L M 1987 Evaluation of an exaggerated somatosensorydeficit with symptom validity testing. Archives of Neurology 44: 798

Poeck K, Luzzatti C 1988 Slowly progressive aphasia in three patients: the problem ofaccompanying neuropsychological deficit. Brain 111: 151–168

10N

euro

psy

cho

log

y

448

Ch10.qxd 20/7/04 8:12 PM Page 448

Reitan R M 1964 Psychological deficits resulting from cerebral lesions in man. In: Warren JM, Akert K (Eds) The frontal granular cortex and behavior. McGraw – Hill, New York,Ch. 14

Russell E W 1982 Theory and developments of pattern analysis methods related to theHalstead–Reitan Battery. In: Logue P E, Shear J M (Eds) Clinical neuropsychology: amultidisciplinary approach. Thomas, Springfield, Illinois, pp. 50–98

Ryan C, Butters N 1980 Learning and memory impairment in young and old alcoholics:evidence for the premature aging hypothesis. Alcoholism: Clinical and ExperimentalResearch 4: 288–293

Shallice T 1982 Specific impairments of planning. Philosophical Transactions of the RoyalSociety of London 298: 199–209

Shallice T 1988 From neuropsychology to mental structure. Cambridge University Press,Cambridge

Shapiro M B 1951 Experimental studies of a perceptual anomaly, 1. Initial experiments.Journal of Mental Science 97: 90–100

Shapiro M B 1973 Intensive assessment of the single case: an inductive deductive approach.In: Mittler P (Ed.) The psychological assessment of mental and physical handicaps.Tavistock Publications, London, Ch. 21

Smith A 1975 Neuropsychological testing in neurological disorders. In: Friedlander W J (Ed.)Advances in neurology. Raven Press, New York, Vol. 7, pp. 49–110

Snowden J S, Goulding P J, Neary D 1989 Semantic dementia: a form of circumscribedcerebral atrophy. Behavioral Neurology 2: 167–182

Talbot P R, Snowden J S, Lloyd J J, Neary D, Testa H J 1995 The contribution of singlephoton emission tomography to the clinical differentiation of degenerative cortical braindisorders. Journal of Neurology 242: 579–586

Walsh K W 1991 Understanding brain damage. A primer of neuro psychological evaluation,2nd edn. Churchill Livingstone, Edinburgh

Walsh K W 1992 Some gnomes worth knowing. The Clinical Neuropsychologist 6: 119–133Walsh K W 1995 A hypothesis-testing approach to assessment. In: Mapou R L, Spector J

(Eds) Neuropsychological assessment of cognitive function. Plenum, New YorkWechsler D 2001 Wechsler Test of Adult Reading. The Psychological Corporation, San

Antonio, TexasWeintraub S, Mesulam M-M 1993 Four neuropsychological profiles in dementia.

Amsterdam: ElsevierWeintraub S, Rubin N, Mesulam M-M 1990 Primary progressive aphasia: longitudinal

course, neuropsychological profile and language features. Archives of Neurology 47:1329–1335

10N

euro

psych

olo

gical assessm

ent

449

Ch10.qxd 20/7/04 8:12 PM Page 449

Ch10.qxd 20/7/04 8:12 PM Page 450