CJ, Re [2009] QMHC 9

MENTAL HEALTH COURT CITATION: Re CJ [2009] QMHC 9 PARTIES: REFERENCE BY THE PATIENT’S LEGAL REPRESENTATIVE IN RESPECT OF CJ PROCEEDING NO: No 0299/07 DELIVERED ON: 28 August 2009 DELIVERED AT: Brisbane HEARING DATES: 11, 12 June 2009 JUDGE: Philippides J ASSISTING PSYCHIATRISTS: Dr J Lawrence Dr E N McVie FINDINGS AND ORDERS 1. There is a reasonable doubt the defendant committed the charges the subject of the references made 11 February 2008 and 27 February 2008, such that no finding is made as to soundness of mind; 2. The defendant is fit for trial; and 3. The proceedings against the defendant in relation to those references and the previous reference are to continue according to law. CATCHWORDS: MENTAL HEALTH – DECLARATION OR FINDING OF MENTAL ILLNESS OR INCAPACITY – where defendant charged with sexual offences – where defendant not of unsound mind – whether defendant fit for trial – whether defendant suffers from significant cognitive impairment Mental Health Act 2000 (Qld), s 27.3(1)(b) Mental Health Act 2000 (Qld), Schedule 2 Kesavarajah v R (1994) 181 CLR 230 Ngatayi v R (1980) 147 CLR R v M [2002] QCA 464 R v Presser [1958] VR 45 COUNSEL: A Lossberg for the Director of Public Prosecutions J Tate for the Director of Mental Health M Green for the Defendant SOLICITORS: Director of Public Prosecutions (Qld) Crown Law for the Director of Mental Health Howden Saggers Solicitors for the Defendant -- 1 of 15 -- 2 PHILIPPIDES J: The Offences [1] The defendant is charged with a number of sexual offences including rape, deprivation of liberty, indecent assault and stupefying in order to commit an indictable offence, between 1986 and 2000. It is alleged that the offences occurred in the context of alleged victims responding to advertisements the defendant placed in the paper for someone to help on a yacht he was sailing around Queensland. [2] The defendant disputes the facts in relation to each of the complaints. He maintains that any alleged sexual conduct with the complainants was consensual. Background [3] In June 2006, the defendant was admitted to the Maryborough Correctional Centre following extradition from South Australia. He was held on remand at the Arthur Gorrie Correctional Centre from June to August 2006, where he was assessed by the Prison Mental Health Service and was noted to be presenting with mania with psychotic symptoms. In view of the need for diagnostic clarification, particularly around organic aetiology, and the defendant’s non-compliance with medication while in custody, he was transferred on 1 September 2006 to the High Security Inpatient Program at The Park Centre for Mental Health and placed on an involuntary treatment order (ITO). [4] Dr Neillie, who reviewed the defendant on several occasions, compiled a report dated 29 January 2007, in which he noted the defendant’s history of heavy alcohol use over a 37 year time period. He also noted that the development of the defendant’s manic episode had occurred against the background of possible longer standing hypomanic features. He made a diagnosis of Bipolar Affective Disorder. He noted that during his inpatient stay, the defendant underwent specific neuropsychological testing over a period of two months, from December 2006 to January 2007, in relation to executive functioning. These investigations, which included EEG and MRI scans, were noted to be unremarkable. A CT brain scan conducted on 7 September 2006 was also noted to show no neurological symptoms. In Dr Neillie’s opinion, the defendant was fit for trial, finding that the defendant understood the nature of the charges and the nature of court proceedings and could explain his account to counsel and the court; the defendant denied the offences, acknowledging the alleged victims had been on his yacht but denying any non- consensual sexual activity. [5] In a further report of 5 April 2007, Dr Neillie noted that the defendant had suffered a deterioration in his mental state in February 2008 in the context of a bail application and an appeal against the ITO. The defendant was commenced on lithium with a noted improvement in his condition. (The ITO was eventually revoked on 31 March 2009). [6] On 13 April 2007, the Mental Health Court heard a reference concerning the charges. The defendant disputed the facts in relation to each of the alleged offences. As the dispute was not attributable to his mental condition, a finding was made that there was a reasonable doubt as to the commission of the alleged offences and no finding was made as to his state of mind at the relevant times. The Mental Health -- 2 of 15 -- 3 Court found that the defendant was fit for trial and ordered that the proceedings continue according to law. An order was also made under the Mental Health Act 2000 (Qld), detaining the defendant to the High Security Inpatient Unit. [7] On 15 May 2007, the defendant was granted bail. [8] On 17 September 2007, the defendant was charged with further offences. [9] His solicitors were instructed to apply for an adjournment of the committal proceedings, so that the defendant could receive treatment from a psychiatrist. According to his solicitor, at a conference on 14 September 2007, the defendant had been unable to provide detailed instructions needed to prepare for the committal proceedings. On 15 September 2007, the defendant was seen by Dr Petchkovsky who conducted some tests and provided a short report. He saw the defendant again two days later. On 17 September 2007, the application for adjournment of the committal proceedings was refused. The defendant attended the first day of the committal proceedings, but on 18 September he provided written instructions that he found the committal proceedings stressful and confusing and believed it was worsening his mental health state. The committal proceeded in his absence until 21 September 2007, when it was adjourned on a referral being made to the Mental Health Court. Dr Petchkovsky’s examination on 15 September 2007 [10] After seeing the defendant on 15 September 2007, Dr Petchkovsky noted the defendant’s complaint as being that: “On Thursday 13 Sept 2007, while briefing his lawyers, he noticed an episode of mental blankness of sudden onset, with a failure of memory (retrieval). This persisted into the next day, when he could not find the rooms of his GP or even remember his name.” [11] Dr Petchkovsky stated that, on assessing the defendant’s mental state on 15 September 2009, he showed strong evidence of early dementia. He noted that on the Mini-Mental State Examination (MMSE), a screening test for cognitive impairment, the defendant’s score was 12/30 and that there was a high score on the DES (Dissociability Scale score of 85 on a range of 0 to 100). He also noted possible prosopagnosia (parietal lobe damage). He reported that the defendant felt his memory has been deteriorating over the last two to three years. Dr Petchkovsky noted that Affective Disorders (including BPAD) are sometimes the harbingers of presenile dementia and that this description could be consistent with dissociation of transient cerebral ischaemia on top of a significant early dementing process. He referred the defendant to Dr Morris, a specialist psychogeriatrician, for a neuropsychiatric assessment and a detailed cognitive/memory assessment. Dr Telang – November 2007 [12] The defendant was an outpatient of the Southport Community Mental Health Clinic from May to November 2007. He was reviewed at the Clinic by Dr Telang, who provided a section 238 report in November 2007. Dr Telang observed that the defendant claimed memory deficits and confusion. His MMSE showed a score of 28/30. Dr Telang noted that the defendant maintained that he was not able to instruct his solicitors “as he does not remember the facts”. He also noted that the -- 3 of 15 -- 4 defendant understood the charges against him and the nature of court proceedings. However, he stated that the defendant could not explain any version of the facts to counsel and the court and could not challenge jurors. He considered the defendant was not then fit to stand trial and, in order to determine whether the defendant was feigning memory deficit, recommended that a greater observation period was required. Dr Morris – 26 November 2007 [13] Dr Morris saw the defendant on 7 and 26 November 2007 and provided a report dated 26 November 2007. He opined that the defendant’s mood disorder could be diagnosed as bipolar affective disorder. However, he also noted that it was unusual for a person to develop such a condition in their late sixties, stating: “… so one needs to consider whether this condition was present earlier in his life. On the basis of my examination of him it was not possible to go back in great detail concerning his psychiatric history earlier than 2006 because of his claimed memory problems. However, Dr Neillie indicates there may have been a history of hypo manic symptoms earlier in his life which indicates the onset of this condition could have started 10-20 years ago. The onset of a manic episode in later life also raises the possibility of an underlying physical or organic condition. He has been investigated to some extent for this possibility when at The Park Mental Hospital and I understand major physical causes of manic symptoms were ruled out at that time.” [14] Dr Morris clearly had some difficulty in assessing the defendant because of his poor cooperation. He noted that the defendant’s current mental status examination was abnormal, in that he claimed little memory for past events and scored very poorly on cognitive screening examinations. On the MMSE given by Dr Morris, the defendant obtained a score of 14/30. Dr Morris noted that: “The poor result on the mini mental state examination reflected poor cooperation with the testing as well as ‘approximate’ answers to many of the questions. His cognitive mental status examination abnormalities raise a number of diagnostic possibilities. He could have developed a dementia syndrome such as Alzheimer’s disease, vascular dementia or stroke related problems. He may suffer from a depression which has affected his ability to respond and cooperate with testing (depressive pseudo-dementia), or he could be in a dissociative amnesic state which limits his capacity to respond appropriately. Alternatively, his response to being asked to provide a history and do a mental status examination may reflect frank malingering or a factitious disorder with predominantly psychological signs and symptoms.” [15] At the time, Dr Morris was of the view that the defendant was not fit for trial, but that the unfitness was a temporary condition only expected to last for some months. He opined that on the “resolution of the factitious disorder he should be again fit for trial”. In the meantime, he recommended the continuation of the ITO. -- 4 of 15 -- 5 Dr Telang – January and February 2008 [16] After Dr Telang had the opportunity to review all of the defendant’s files and the report of Dr Neillie that he had not previously seen, he revised his opinion as to fitness for trial and provided an addendum, dated 18 January 2008, to his report stating that he considered the defendant to be fit for trial. He confirmed that view in his report of 19 February 2008. Dr Ng – May 2008 [17] In April 2008, the defendant was transferred to the Aged Care Mental Health Services and reviewed by Dr Ng, who reported on 8 May 2008 that the defendant still maintained he had extensive autobiographical memory deficits. He had been travelling north to meet friends and relatives in order to “jog” his memory (apparently on the advice of his private psychiatrist). The defendant denied any knowledge of the charges pending, but could understand the meaning and implications of them and maintained his innocence. On questioning of his autobiographical memory, the defendant could not recall his place of birth, his primary school or secondary school, the name of his parents, siblings, wife, or his financial situation. He could not recall any business he had previously been involved with or any business associates. Nevertheless, on reviewing the defendant, Dr Ng was of the opinion that the defendant was fit for trial. Dr Petchkovsky – 2 June 2008 [18] In a report dated 2 June 2008, Dr Petchkovsky stated that he had been treating the defendant since 15 September 2007, when he presented with depression, with anxiety, agitation, suicidality and cognitive difficulties, which made it impossible for him to instruct counsel and attend court meaningfully. Dr Petchkovsky indicated that he had obtained a second opinion from Dr Morris, with a comprehensive cognitive assessment which included CT and SPECT scans. He stated: “Both Dr Morris and I felt, and continue to feel, that we are dealing with a depressive condition with a significant cognitive impairment component. There may also be a Ganser Syndrome component (it is important for the Court to be aware that a diagnosis of Ganser syndrome does not imply factitiousness, since patients with a Ganser presentation are often quite unconscious of their process). It is not possible to establish at this stage if there is also an early prodromal dementing process at work, though given the strong linkage between depression and Alzheimers’ in the elderly, an early dementing component would be likely.” [19] He stated that he had been treating the defendant regularly (with anti-depressants and supportive psychotherapy), and that the defendant had made great improvements. Nevertheless, he considered that the defendant remained vulnerable and at risk under the stress of trial conditions of serious relapse and hospitalisation. He was of the view that, given a prolonged period of consolidation of about one year, the defendant’s mental health would become robust enough to withstand trial conditions. [20] In a further report on fitness for trial, he stated: -- 5 of 15 -- 6 “My final view then is as follows. [CJ] has BPAD I. [CJ], a right handed individual, also has left (Dominant hemisphere) temporal lobe atrophy, secondary to organic trauma. The dominant temporal lobe plays a central role in (i) the recognition and understanding of language (ii) memory and new learning (via the hippocampus) (iii) emotionality (via temporal and hippocampal projections to amygdale and limbic system), and even, in its upper region (superior temporal lobe, angular gyrus) to aspects of recognition broader than verbal/lexical ones. (In [CJ]’s case, there is a recurrent prosopagnosia, a forgetting of faces). This has resulted in a significant cognitive defect, affecting mainly memory functions. [CJ] has made an adaptation to this deficit over the years. His higher than average pre-morbid intelligence has helped. He has developed a range of coping strategies (including simplifying his life-style and using little note-books, in which he jots down names, times, items and tasks to remember). Residual neuroplasticity has also recruited some right Temporal lobe function, so that under optimal conditions, and in combination with the above strategies, he functions well enough to manage activities of daily living (DOIDGE 2007). However, whenever he is placed under any stress, he decompensates visibly. Neuroplastically recruited brain functions are always brittle, and collapse under stress. His PBAD contributes to this vulnerability.” Dr Douglas – 7 October 2008 [21] Dr Douglas, a psychologist, provided a report dated 7 October 2008, having examined the defendant on 14 August 2008. Dr Douglas observed that at interview the defendant presented as “fluent and articulate in casual conversation” but that when formal testing was attempted, he insisted that he could not “read, write, spell, count or recognise shapes or letters”. Dr Douglas considered the discrepancy between the defendant’s actual presentation and purported cognitive abilities “bizarre, extreme and completely inconsistent with the presence of any objective cognitive dysfunction”. She also observed as “of particular note that [CJ]’s apparent onset of a global amnestic disorder that has obliterated his personal history begins in September 2007 once he is before a committal hearing, and in the complete absence of any identified severe neuropathy”. [22] Dr Douglas considered the defendant’s performance on a number of psychometric tests was “uniformly indicative of a gross exaggeration of likely cognitive dysfunction”. By way of example, Dr Douglas noted that the defendant achieved a combined score of 6/30 on the Rey 15 item test, whereas individuals diagnosed with mental retardation can obtain scores of 11/30 on that measure. Moreover, she noted that the defendant was the only individual she has encountered in 25 years of psychometric testing to achieve a score of 0/15 on the Rey Free Recall test. On the TOMM the defendant achieved scores of 32/50 on Trial 1 and 33/50 on Trial 2. Dr Douglas considered that the defendant’s abnormally low scores on a range of psychometric tests indicated that he was not fully cooperative with the process and that as such his scores on these measures could not be used to “accurately and reliably determine … [his] actual level of cognitive functioning”. [23] Dr Douglas opined that the defendant was fit for trial, stating: -- 6 of 15 -- 7 “There is no objective evidence of any memory impairment … and as noted previously the supposed onset of his complete loss of autobiographical memory is bizarre, inconsistent with his behavioural presentation and not supported by formal cognitive evaluation.” Dr Byrne – 13 October 2008 [24] Dr Byrne saw the defendant on 4 September 2008. In his report of 13 October 2008, Dr Byrne stated that on the MMSE the defendant scored 10/30. He noted that scores of 24 or less are generally considered indicative of clinically significant cognitive impairment and that scores of 18 or less are commonly seen in patients with dementia of at least moderate severity. Dr Byrne considered that the defendant’s test-taking behaviour was abnormal with an excessive number of near miss and “don’t know” responses. He noted that in Dr Telang’s report of November 2007 the MMSE score was 28/30 which was a normal performance. Dr Byrne stated: “A decline of 18 points in less than one year on this test could only be attributable to a catastrophic organic mental disorder, of which there is no evidence in the present case. By comparison, patients with the progressive dementing disorder, Alzheimer’s disease, decline by two or four points on the MMSE each year.” [25] Dr Byrne also noted that the CT brain scan performed on 7 September 2006 was reported as normal and that an MRI brain scan performed in November 2007 was reported as showing “a mild prominence of the ventricles, basal cisterns and sulci”. A further MRI brain scan was performed on 11 February 2008, which was reported as showing “apparently isolated left temporal lobe atrophy”. He further noted that a radionuclide SPECT brain scan was performed on the same day and showed “marked reduction of perfusion of the left temporal lobe”. [26] In respect of the clinical findings, Dr Byrne concluded in his report as follows: “In my opinion, ?CJ exhibits the clinical picture of exaggerated cognitive impairment with approximate answers and pseudodementia. He has a history of a prolonged manic episode, which is likely to be due to late-onset bipolar disorder. This is currently in remission. He also has a history of longstanding heavy alcohol intake that is likely to represent alcohol abuse and dependence. These are currently in remission. In my view, the differential diagnosis of [CJ]’s current presentation includes malingering, factitious disorder, dissociative disorder and organic brain syndrome. I favour the first two possibilities but cannot completely exclude some component of the latter two. The recent MRI brain scan shows a left temporal lobe that is smaller than the right temporal lobe. This may represent a normal variant, as the left temporal lobe is commonly smaller than the right temporal lobe. Alternatively, it might be evidence of previous brain damage (but there is no gliosis), evidence of previous stroke (but there is no -- 7 of 15 -- 8 other evidence of cerebrovascular disease) or evidence of a neurodegenerative condition (this is more difficult to exclude, although the available history does not suggest this). The corresponding reduction in cerebral perfusion on the SPECT brain scan undertaken on the same day adds no further information because localised loss of brain volume is inevitably associated with reduced cerebral blood flow in the same region. Alternative, and more likely, types of brain damage in this case, which would be unrelated to the apparent brain scan findings, are amnestic disorder and frontal lobe damage due to longstanding alcohol abuse or dependence. I am not convinced that these are present and the report from Dr Darren Neillie suggests that they are not. However, even if these organic mental disorders were present to some degree, the current clinical findings suggest an exaggerated presentation. However, on balance I think it most likely that [CJ] is acting as if he has an illness, in this case dementia, by deliberately producing or exaggerating symptoms of cognitive impairment. He may hope to gain sympathy or leniency by adopting this illness behaviour and its associated sick role.” [27] In giving evidence, Dr Byrne stated that there were four possibilities to explain the many inconsistencies. The differential diagnosis was malingering, factitious disorder, dissociative disorder and organic brain syndromes. Dr Byrne favoured the view that the defendant was malingering, pointing to a number of examples to illustrate that position. Dr Byrne concluded that the defendant had developed an abnormal pattern of behaviour that represented an attempt to mimic severe cognitive impairment or dementia. [28] In respect of fitness for trial, his opinion was as follows: “…[CJ] is probably fit for trial although his current mental state, if taken at face value, suggests that he is not. [CJ] was able to follow my instructions and appeared to understand my questions, even if he provided ‘don’t know’ responses to most of them. He appeared to make his way to my 8th floor rooms unaided and cooperated superficially with my interview. He apparently attends his treating psychiatrist and case manager on a regular basis. He was able to recall the names of his prescribed medication, the number of tablets he takes and the pattern of taking his medication. He was able to recall the results of his recent brain scans and he was able to tell me that his treating psychiatrist thought he had had a stroke. He appreciated that it was thought his left temporal lobe was smaller than the right. [CJ] would not answer specific questions in relation to the charges, however this does not necessarily mean that he does not understand the charges. -- 8 of 15 -- 9 He answered my questions quickly even though his answers often contained little information. [CJ] did provide answers to some of my questions on the operation of the Court. He appeared to understand the roles of the officers of the Court, including the judge, barrister and prosecutor. However, he responded ‘don’t know’ to my question on the role of the jury. It seemed unlikely to me that he would understand the roles of officers of the Court but not the role of the jury. It seems unlikely that [CJ] would misbehave in Court, but if his present behaviour persisted then he would not cooperate with Court proceedings. I have no reason to believe that Court proceedings would be any more distressing to [CJ] than to any other person charged with similar offences. I think it is likely that with the assistance of counsel [CJ] would be fit for trial, although I am aware that others have come to a different view about this. In relation to Q v Presser one remaining issue in my mind is whether [CJ] has the capacity to make his version of the facts known to the Court and to his counsel. I think it is more likely than not that he has that capacity, but currently chooses not to exercise it.” Dr Coyle – 27 November 2008 [29] Dr Coyle conducted a number of psychometric tests on the defendant on 15 October 2008. The TOMM scores were 18/50 on Trial 1 and 21/50 on Trial 2. On the Rey 15 the defendant scored 3/15. On the ACE he scored 16/100. On the MFAST he scored 3/25. In his report of 27 November 2008 Dr Coyle concluded: “Doing the best I can I am of the view that some of his behaviour is typical of Gansers Syndrome; some is clear exaggeration and some is genuine. I have no idea how any lawyer could hope to receive comprehensible instructions from [CJ] considering this situation. Even if the overwhelming majority of his behaviour could be attributed to motivational factors the fact is that at least some of his behaviour could be attributed to other factors. And there is no getting around the fact that he has demonstrable neurological insult. The problem is determining exactly what elements of his presentation are due to neurological insult. Since there is no way of ascertaining this during conference with legal counsel and during the course of a trial. I am therefore of the view that he’s not therefore fit to plead in accordance with the Presser rules.” Dr Morris – 28 November 2008 [30] Dr Morris provided a further report of the defendant in November 2008, after he had the opportunity of reading the reports of Drs Byrne, Telang, Petchovsky and Douglas. In that report, he stated that the February 2008 MRI scan showed significant atrophy of the left temporal lobe and hippocampus, and that the SPECT -- 9 of 15 -- 10 scan showed a marked reduction in perfusion in the left temporal lobe, both including and extending beyond the hippocampus on that side. He opined that: “These findings are of considerable importance because the left temporal lobe and associated hippocampus is responsible for the integrity of narrative or episodic memory function – the abnormality that [CJ] complains of and demonstrates on testing. The cause of these abnormalities is not entirely clear. They could be the result of previous head trauma, a congenital or developmental abnormality, cerebral vascular insults, or early degenerative disease of the brain … among other possibilities.” Dr Hodges – 17 February 2009 [31] Dr Hodges, a professor of cognitive behaviour neurology, reviewed the MRI brain scan and the SPECT scan of 11 February 2008. In a report of 17 February 2009 he noted: “The MRI shows mild but significant atrophy involving the left hippocampus. This is evident from enlargement to the temporal horn of the left lateral ventricle particularly in the axial images. There is also a degree of atrophy involving the other structures in the left temporal lobe. In keeping with the MRI, the SPECT scan also shows perfusion abnormalities involving the left temporal lobe. There is a reduction in blood flow, particularly affecting the left hippocampus but extending beyond to incorporate other parts of the left temporal lobe. I would stress that a diagnosis of dementia is a clinical one and is based upon history and cognitive examination. Brain imaging is performed to investigate the potential cause of dementia rather than to establish whether a patient does or does not suffer from cognitive impairment.” [32] Dr Hodges could not rule out some possible frontotemporal dementia, but indicated one would expect greater deterioration than apparent in this case from the scans. He did not consider that an individual with the appearance evident from the defendant’s scans to have severe memory loss. Dr Hodges did not consider the concept of neuroplasicity as pertinent and did not give it any credence as a factor having any relevant operation in the present case. Dr Hearn – 23 March 2009 [33] Dr Hearn saw the defendant for a neuropsychological assessment on 19 and 24 March 2009. The testing included a MMSE, on which the defendant scored 12/30. Other tests administered included the WAIS-III, the D-KEFS and the Cognisat. To formally assess the defendant’s motivation, effort and the likely validity of his test performance, the TOMM and Rey 15 were administered. The defendant’s performance on both of those tests was considerably below the expected normative level. Dr Hearn considered that the results raised serious concerns as to whether the defendant was putting maximum effort into the neuropsychological tests. -- 10 of 15 -- 11 [34] In his report of 23 March 2009, Dr Hearn stated that, taking all of the extensive information into consideration, it was possible to conclude that the defendant was experiencing some reduction in memory functioning associated with the changes seen on the SPECT and MRI scans. However, due to the defendant’s results on tests of motivation and effort, along with inconsistencies in his presentation, Dr Hearn considered it likely that the extent of any memory deficits was being “greatly over inflated by a lack of effort” during formal assessment. Additionally, it was noted that the pattern of cognitive deficits the defendant described and showed on formal testing was highly unusual and did not fit “the typical pattern of cognitive deficits seen in cases of dementia due to organic causes”. Dr Hearn considered that the inconsistencies and lack of application on formal testing could be explained in terms of conscious exaggeration or some psychological disorder such as hysterical pseudodementia, and she was unable to offer a definitive clinical view as to which position should be preferred. However, Dr Hearn on balance appeared inclined to the view that the defendant did meet the Presser standards and was fit for trial based on a number of observations, including his assessment of the defendant’s results on tests of effort and motivation, and his general presentation during assessment. Dr Morris – 15 May 2009 [35] Dr Morris examined the defendant on 6 May 2009 and conducted a cognitive examination which included the ACE-R (embedded within which is the MMSE) and the TOMM. The defendant’s MMSE score was 19/30 and his ACE-R score was 43/50, well below the suggested cut off for patients with dementia. Dr Morris administered three trials of the TOMM, on which the defendant scored 33/50, 38/50 and 40/50. Dr Morris accepted that a score of less than 45 on the second or third trial raised concerns that the individual was not putting forth a maximum effort and may be malingering. However, he concluded that although the defendant’s scores were below 45 on all three trials, there was a learning effect present whereby his score improved from 33 to 40. Dr Morris observed that individuals who are fabricating or malingering usually score quite poorly and do not improve on subsequent trials. [36] Dr Morris noted the differences of opinion that had emerged between the experts who had examined the defendant as to the nature, extent and cause of his cognitive difficulties. He observed that on the one side were those who considered that the defendant’s cognitive problems were fabricated or conscious attempts to feign cognitive impairment, while on the other side were those who considered that there was an underlying organic brain disease or unconscious psychological processes leading to cognitive impairment. Dr Morris opined that an alternate view was that the defendant had a core cognitive deficit, based on underlying organic brain conditions, with the extent of impairment being variable due to factors affecting test taking effort or cooperation, such as anxiety, stress and potential secondary gain. Dr Morris noted that there had been an improvement in cognitive capacities over the previous 18 months as measured by the defendant’s performance on the MMSE and TOMM as compared with the testing conducted by Drs Douglas and Coyle. [37] Dr Morris also observed: “The underlying organic conditions that cause the core component of his cognitive impairment have not been fully determined. Gradually progressive degenerative diseases of the brain such as Alzheimer’s disease or frontotemporal dementia are the most likely possibilities. -- 11 of 15 -- 12 I note that the MRI scan done in November 2006 also showed atrophy of the left temporal lobe that was found in the MRI scan done on 11.2.08. This finding would indicate a chronic process that may be contributing to his cognitive impairment. Another possibility is that he suffered from the cognitive and memory disturbance associated with longstanding heavy alcohol dependence. Long term heavy use of alcohol can cause persistent amnestic disorder characterised by the impairment of the ability to learn new information and the inability to recall previously learned information. Another possibility is a combination of alcohol caused memory difficulties combined with an ongoing degenerative disease of the brain such as Alzheimer’s disease or frontotemporal dementia.” [38] In relation to the issue of fitness for trial in terms of the Presser test, Dr Morris considered that the defendant understood the nature of the charges and was able to plead to them, noting that the defendant maintained he was not guilty and denied the charges, asserting that any sexual conduct was consensual. He considered the defendant would be able to answer the charges against him. The defendant also understood the nature of a court and the roles of the court officers, and was aware of the purpose of a trial. However, Dr Morris considered that it would be difficult for the defendant to follow the course of the proceedings given the nature of his cognitive impairment, particularly his difficulties with memory retention and recall, problems with new learning, and problems with abstract reasoning, problem solving and poor judgment. He considered the defendant would have difficulty understanding the substantial effect of the evidence given at a trial. Fitness for Trial [39] Schedule 2 of the Mental Health Act 2000 (Qld) (“the Act”) defines the expression “fit for trial” as meaning: “... fit to plead at the person’s trial and to instruct counsel and endure the person’s trial, with serious adverse consequences to the person’s mental condition unlikely.” [40] The test for determining fitness for trial set out in R v Presser [1958] VR 45, was approved in Kesavarajah v R (1994) 181 CLR 230 at 245 by Mason CJ, Toohey and Gaudron JJ who said: “In R v Presser, Smith J elaborated the minimum standards with which an accused must comply before he or she can be tried without unfairness or injustice [1958] VR 45 at 48. Those standards, which are based on the well-known explanation given by Alderson B to the jury in R v Pritchard (1836) 7 Car & P 303 at 304; 173 ER 135 at 135, require the ability (1) to understand the nature of the charge; (2) to plead to the charge and to exercise the right of challenge; (3) to understand the nature of the proceedings, namely, that it is an inquiry as to whether the accused committed the offence charged; (4) to follow the course of the proceedings; (5) to understand the substantial effect of any evidence that may be given in support of the prosecution; and (6) to make a defence or answer the charge.” -- 12 of 15 -- 13 [41] In R v M [2002] QCA 464, the Court of Appeal applied the Presser test in respect of the statutory definition in the Act. The Court held that in approaching the issue of fitness for trial, regard is also had to the fact that a defendant is represented by counsel; accordingly it is not necessary that a defendant understand the nuances of court procedure or the intricacies of substantive law (at [5]). Rather fitness for trial should be assessed in the recognition that a defendant is represented by counsel and that court proceedings may be structured in order to accommodate disability (at [7]). As the High Court stated in Ngatayi v R (1980) 147 CLR 1 at 8, a reasonable and commonsense approach is to be taken to the application of the Presser criteria. Conclusion [42] The evidence clearly indicates that the defendant suffered from a psychiatric condition exhibiting manic symptoms which resulted in the making of an ITO which was subsequently revoked. However, the defendant was considered fit for trial after various evaluations, including MRI and ECG investigations, and close examination by mental health services. The picture changed somewhat dramatically in September 2007 in the context of the defendant instructing solicitors prior to committal proceedings, when the defendant experienced a sudden mental blankness and failure of memory. This was described by Dr Petchkovsky who performed a MMSE wherein the defendant scored the astonishing result of 12/30. However, some two months later Dr Telang administered the test with a result of 28/30 being achieved, that is largely within normal range. [43] Further investigations were carried out and Dr Hodges gave evidence after examining the MRI and SPECT. I note that Dr Hodges’ clear evidence was that the question of the existence of dementia is one to be determined by clinical assessment rather than an analysis of the scans. However, he did indicate that he would not expect someone with the defendant’s appearance to have severe memory loss and he would not expect someone with this appearance on a scan to have problems retaining information as the defendant claimed to be experiencing. While he accepted that the scans could be consistent with a degenerative condition, the most likely candidate being an early onset Alzheimer’s dementia and possibly a frontotemporal dementia, he noted that there was no frontal lobe degeneration. [44] Drs Petchkovsky, Morris and Coyle were of the opinion that there was an organic brain disorder present which caused significant cognitive disability, such that the defendant was unfit for trial. [45] In advising the court on the clinical evidence, Dr McVie noted that: “the diagnosis of an early Alzheimer’s would be consistent with a previous scan in November 2006 showing some deterioration of the left temporal lobe, although less deterioration than the February ‘08 scans, and this evidence was reported by Dr Morris who said that he had had the earlier scans reviewed by his radiologist, though we do not have this information in writing. … [However] Dr Byrne gave clear evidence which supported Professor Hodges’ view that a diagnosis has to be made clinically and the scan may support it. He said that the memory deficits described did not fit any pattern of a dementing illness. Dr Byrne also agreed that bilateral temporal lobe involvement is usually -- 13 of 15 -- 14 required for significant impairment of the memory. The widespread cognitive defects as described were unlikely to be explained by such a lesion as the isolated temporal lobe atrophy.” [46] A concern in the present case is the variation referred to in detail above in the MMSE scores over the period from November 2006 to May 2009. I note that Dr Byrne considered it difficult to conceive of any condition which would result in such a marked deterioration in scoring over such a period. [47] In advising the court as to the significance of the evidence of Drs Petchkovsky, Morris and Coyle, Dr Lawrence stated: “In my opinion, those reporters are not paying sufficient attention to the extensive descriptions of inconsistencies in performance, both the behaviour of [the defendant] … in his day-to-day functional assessments, his every day living abilities, which we have heard about.” [48] I note that Dr Petchkovsky was strongly of the view that the defendant was unfit for trial. I must say that I considered the value of his evidence to be compromised by the manner in which he gave it, which was more akin to that of an advocate for the defendant. I note that his concepts of the operation of neuroplasticity were discounted by Dr Hodges. In commenting on the evidence given by Dr Morris, Dr Lawrence observed that his opinion that the defendant suffers from very severe cognitive deficits resulting in unfitness, largely stemmed from “translating the results of rather limited testing which others haven’t been able to consistently find reliable into the medical situation”. In relation to the views postulated by Dr Morris’ on the basis that there had been some improvement in the defendant’s scoring, Dr McVie commented: “… I note Professor Morris who said that … the scores had improved and he was making some suggestions as to diagnosis based on his scores, but the scores were still low, and even the TOMM that he administered was still below the cut-off point of 45, which I would consider the neuropsychologists would advise makes it very unwise to interpret results of any other tests if a score of below 45 is achieved on the TOMM.” [49] The evidence indicated that there were marked differences between the defendant’s clinical presentations when compared with his test scores. In respect of this aspect, I note the comments of Dr McVie that: “Drs Byrne, Hearn and Douglas were perhaps the clearest in reporting these discrepancies. An example would be his ability to be able to communicate in general conversation, to ride a motorcycle, and to follow directions which would be completely incompatible with his not being able to read or write or recognise his own name.” I also note Dr McVie’s additional observations concerning the evidence: “There is, however, an inability to completely exclude any underlying organic process such as early Alzheimer’s, but the extreme lack of cooperation with neuropsych testing has resulted in an inability to quantify any real cognitive deficits that [CJ] may actually have, and though there might be an element of unconscious -- 14 of 15 -- 15 process or psychological overlay, the marked secondary gain in avoiding being found fit for trial in this case is very obvious.” [50] In relation to the issue of malingering, I found the following comments of Dr McVie of assistance in considering the evidence as a whole. They also go to illustrating why I ultimately found the views expressed by Dr Byrne and Dr Douglas persuasive. Dr McVie commented as follows: “I would consider the facts pointing to malingering include the marked inconsistencies between his observed behaviour and communication interview and his behaviour in results during the formal testing, the marked inconsistency between his symptoms and any identified cognitive deficits with any known neuropsychological syndrome, the approximate answers as described by Dr Byrne give a very clear example of, and they do suggest that he does have adequate skills in understanding and answering questions, and the neuropsychological tests, the TOMM and the Rey 15, which indicates poor effort and they are valid for detecting poor effort and the findings on these tests do invalidate the results of the other cognitive tests. Also Dr Byrne’s comment in evidence that it’s unusual for factitious disorder to present solely with memory problems and usually a factitious disorder arises in the context of a need for care and treatment. Dr Douglas in her evidence also said that her results excluded any hypothesis of organic brain damage dissociative disorder or any psychological disorder.” [51] I note that counsel for the defendant did not press a submission that the defendant was permanently unfit for trial, rather it was urged that a finding of temporary unfitness be made pending further clarification of the defendant’s position. However, having considered the vast amount of clinical material and the evidence presented, I am of the view for the reasons outlined that the views of Drs Byrne and Douglas are to be preferred over those of Drs Petchkovsky, Morris and Coyle. I found Dr Byrne’s distinction between malingering and factitious disorder lucid and compelling, as I did his reasoning for concluding that the defendant was malingering and fit for trial. I am satisfied that that determination ought to be made and find on the balance of probabilities that the defendant is fit for trial. Orders [52] In relation to the reference that was previously before the court on 13 April 2007, I find that the defendant being fit for trial, the proceedings the subject of that reference are to continue according to law. In relation to the subsequent reference of charges, I find that there is a dispute of fact not attributable to the defendant’s mental condition, such that there is a reasonable doubt that he committed the alleged offences. I also order that the defendant being fit for trial, those proceedings continue according to law. -- 15 of 15 --