Re Ma'a
[2010] QMHC 6
•30 April 2010
MENTAL HEALTH COURT
CITATION:
Re Ma’a [2010] QMHC 006
PARTIES:
REFERENCE BY THE DEFENDANT’S LEGAL REPRESENTATIVE IN RESPECT OF PAULO MA’A
PROCEEDING NO:
No 0174 of 2008
DELIVERED ON:
30 April 2010
DELIVERED AT:
Brisbane
HEARING DATE:
20, 21 April 2010
JUDGE:
Philippides J
ASSISTING PSYCHIATRISTS:
Dr E N McVie
Dr F Varghese
FINDINGS AND ORDER:
1. The defendant was not of unsound mind as described in Schedule 2 of the Mental Health Act 2000 (Qld) at the time of the commission of the alleged offence;
2. The defendant was not of diminished responsibility as described in Schedule 2 of the Mental Health Act 2000 (Qld) in relation to the offence of murder;
3. The defendant is permanently unfit for trial;
4. The defendant be detained to The Park High Security Program Authorised Mental Health Service.
CATCHWORDS:
MENTAL HEALTH – DECLARATION OR FINDING OF MENTAL ILLNESS OR INCAPACITY – where defendant charged with murder and serious assault – where defendant suffered from frontotemporal dementia – whether defendant suffered from a mental disease – whether defendant was of unsound mind as defined in Schedule 2 of the Mental Health Act 2000 (Qld) at the relevant times – whether in relation to the charge of murder the defendant was of diminished responsibility – whether defendant is fit for trial.
Mental Health Act 2000 (Qld), Schedule 2
COUNSEL:
Mr J Briggs for the Defendant
Mr J Tate for the Director of Mental HealthMs S Bain for the Director of Public Prosecutions
SOLICITORS:
Legal Aid Queensland for the Defendant
Crown Law for the Director of Mental HealthThe Director of Public Prosecutions (Qld)
PHILIPPIDES J:
The defendant, Paulo Ma’a, is charged with the murder of Isaako Sala on 3 January 2007 and also with serious assault on 4 January 2007. The matter of the defendant’s mental state at the relevant times has been referred to this Court.
The court is required to determine whether the defendant is of unsound mind as defined in Schedule 2 of the Mental Health Act 2000 (Qld). If the finding is that the defendant was not of unsound mind, the court is required, in relation to the charge of murder, to further consider whether the defendant was of diminished responsibility. The defendant’s fitness for trial is also to be determined.
An initial issue arises as to whether at the relevant times the defendant suffered from a mental disease. In addressing the issues before the court, the court has had the benefit of expert reports from Drs Schramm, Keane, Fama, Byrne, Wilcox and Morris, who all gave oral evidence.
Background
The defendant was born in Samoa and was reported to have moved to New Zealand from Samoa in 1979 with his wife, where he lived until moving to Australia in 1989. The defendant worked as a carpenter in New Zealand and Australia and began working in a factory after moving to Queensland from Melbourne in 2003. He has limited ability to understand and communicate in English.
At the time of the events in question the defendant was 62 years of age. He had been living with the victim for a short period of time. The defendant had presented at the home of a pastor on the evening of 29 December 2006. He told the pastor’s son that he needed help with his car. He had informed the pastor that his name was Tasi Tolo and that he had come from Los Angeles (both of which were untrue). The defendant asked to stay the night. The defendant’s wife reported that the defendant had disappeared after attending church on 30 December 2006. He left having locked his car and saying that he was “going for a walk”. She indicated that he had “disappeared” on previous occasions.
The victim’s brother reported that on 1 January 2007 the victim and defendant had been seen speaking amicably and singing hymns together. On 2 January 2007 the defendant was reported to have been seen by a neighbour carrying several items from the victim’s house. During the early morning of 3 January 2007 witnesses reported hearing raised male voices coming from the scene of the offence. The victim was found by his brother that evening. He had sustained severe head and facial injuries caused by force with a blunt instrument. The defendant and victim are reported to have been seen together at the victim’s house on the day prior to the offence.
On the morning of 3 January 2007, the defendant boarded the Rockhampton tilt train from Roma Station in Brisbane without a ticket. After having apparent health difficulties the defendant was removed from the train at Landsborough. Apparently the defendant’s left arm appeared to be limp and he clutched at his throat and shoulder and was unresponsive to questioning. He was taken to Caloundra Hospital where no serious health problems were detected. He was seen by Dr Pothapu, who noted the defendant had a fast pulse, an elevated temperature (38 degrees) and was "confused". He later told the doctor that the previous night he had drunk a lot of whiskey and had fallen down stairs, which caused pain in his left shoulder. He said he wanted to get back on the train and go home to Cairns. When the defendant’s confusional state worsened a CT scan was performed. He absconded but was brought back by a staff member.
The defendant was transferred to the Nambour Hospital where he was seen by Dr Dobson, who noted that while the defendant did not speak English as a first language, he could make himself understood and could understand spoken English. The defendant was thought to have an underlying rheumatological problem and was medically discharged.
At about 2.00 am on 4 January 2007, police officers from Logan spoke with the defendant. Suddenly, the defendant raised an oxygen cylinder above his head in a threatening manner. He said at various times, “They are trying to kill me”, “I kill you. I kill you”, and “You kill me, you kill me. They kill me, they kill me”. The defendant was arrested and charged with murder later that day.
Dr Davison, a psychiatrist with Prison Mental Health, reviewed the defendant on a number of occasions. He was able to provide some family details including a family history of bipolar disorder. He also elicited a history of three distinct periods of elevated mood lasting six months, associated with heavy drinking.
Clinical evidence
MRI and SPECT scans
An MRI scan was performed on 10 December 2008 and the findings were as follows:
“There are several scattered supratentorial deep white matter foci of FLAIR hyperintensity that number towards the upper limits of normal for the patient’s age. These are non-specific but can be associated with accelerated small vessel cerebrovascular disease and correlation with atherosclerotic risk factors is suggested. The remainder of the cerebral hemispheres, cerebellum and brain stem have a normal appearance. The ventricles and basal cisterns are normal. There is no marked or definite abnormality or asymmetric enlargement of the frontal lobe sulci to suggest a frontotemporal dementia. Normal intracranial flow voids. No restricted diffusion on DWI to indicate acute infarction.”
On 6 March 2009 a CT scan was performed. In the report the following findings were noted:
“There is a generalised moderate reduction of tracer suggesting reduced cerebral perfusion throughout bilateral frontal and temporal lobes, more marked anteriorly, and the bilateral basal ganglia.
Tracer uptake within the parietal, occipital lobes and the cerebellum is unremarkable.No significant atrophy is seen in these regions on the fusion CT, therefore more suggestive of early to mid stage disease rather than end stage disease.
COMMENT:
Scintigraphic appearance is suggestive of frontotemporal type of dementia (FTD). A neurological specialist opinion is suggested.”
A further CT scan was performed on 19 February 2010, the report of which noted the following:
“Comparison is made with the previous brain SPECT study performed 06.03.09.
There is interval development of focal areas of reduced cortical uptake in the right frontal and temporal lobes, as well as further deterioration in the appearance of the left temporal lobe.
New focal reduced uptake at the left parietal lobe.
However, cortical uptake in the remaining parietal and occipital lobes is relatively preserved when compared to the frontal and temporal regions.
COMMENT:
Scintigraphic appearances suggest progression of frontotemporal type dementia over the past year.”
Dr Keane’s evidence
Dr Keane, a clinical neuro-psychologist, provided two reports, one dated 11 March 2008 and the other dated 27 April 2009, after examining the defendant with the assistance of an interpreter.
On 4 March 2008, Dr Keane administered various psychometric tests, the results of which she outlined in her report dated 11 March 2008. The tests administered included the Wechsler Adult Intelligence Scale, Third Edition (WAIS-III), the Dementia Rating Scale (DRS-2), the Reynolds Intelligence Adult Scale (RIAS) which was chosen because it is less gender and ethnic specific and does not rely on the subject reading instructions, the Wide Ranging Assessment of Memory and Learning, and the Test of Memory Malingering (TOMM).
Dr Keane found that the defendant’s scores on the RIAS indicated his verbal IQ was 61, his non-verbal IQ was 78 and his full scale IQ was 65. The defendant’s non‑verbal functioning and executive functioning fell in the “extremely low range”. She stated that the defendant’s assessment of thinking and reasoning abilities measured by the Composite Intelligence index placed him in the extremely low range, which indicated that his level of intellectual ability is in the mental retardation range.
On her testing, the defendant’s memory functioning was also found to fall in the extremely low range. Dr Keane noted that the defendant’s performance on the TOMM did not show any deliberate reduced effort. On the Dementia Rating Scale the defendant’s score fell in the “severely impaired range”, with impaired functioning being evident in initiation/perseveration, conceptualisation and memory tasks. Dr Keane concluded that the defendant’s cognitive profile was most consistent with mild mental retardation and a dementing disorder. However, she considered that the defendant would require a repeat assessment in 12 months to confirm deterioration arising from the latter.
Dr Keane examined the defendant again on 17 April 2009 for her report of 27 April 2009. She reported deterioration in neuropsychological performance, suggesting a progressive neurodegenerative disease. Dr Keane noted that in relation to the dementia rating scale, consistently with her previous assessment, the defendant achieved a total score in the severely impaired range and his performance on tests of attention and concentration also fell within the severely impaired range. The defendant’s memory functioning remained in the extremely low range.
Dr Keane diagnosed Dementia Not Otherwise Specified and mild mental retardation. She also agreed with the diagnosis of frontotemporal dementia made by Dr Fama. She noted the SPECT scan report of 6 March 2009 and MRI report that were provided and reported:
“On assessment, it was difficult to demonstrate overall reduction in functioning across all cognitive domains because of Mr Ma’a’s functioning in the Extremely Low Range on initial assessment. However, Mr Ma’a did demonstrate deterioration in functioning as measured by the Dementia Rating Scale.”
In relation to fitness for trial, Dr Keane concluded:
“… Mr Ma’a is not fit for trial by reason of his Extremely Low Intellectual functioning and Dementia. Mr Ma’a’s cognitive functioning is consistent with that seen in the context of frontotemporal dementia. He has significant deficits across all domains of cognitive functioning, and these cognitive deficits indicate that Mr Ma’a would have substantial difficulty following generally the nature of the proceedings. It would adversely impact on his ability to follow the course of the proceedings so as to understand what is going on in court in a general sense. I also think that his deficits would adversely impact his ability to understand the substantial effect of any evidence that may be given against him. He would not be able to make his defence or answer the charge. I think that the deficits elicited on testing indicate that he does not have sufficient capacity to be able to decide what defence he will rely on and to make his defence and his version of the facts known to the court and to his counsel.”
Dr Keane opined that because of the defendant’s extremely low intellectual functioning and dementia, the defendant did not have sufficient capacity to be able to make a defence and to state to the court and his counsel his version of the facts, and that he would have substantial difficulty following proceedings or understanding the substantial effect of any evidence that might be given against him.
In oral evidence, Dr Keane expanded on the defendant’s “profound difficulty with his working memory”. She reiterated her view that the defendant would have difficulty in meeting the Presser criteria, especially the ability to follow the course of the evidence and make a defence, given his problems with memory and his apathy. He would have difficulty instructing counsel because of his inability to distinguish his memory of the events in question from what he had been told and his difficulty in remembering to relay relevant information to his counsel. She considered that the defendant’s unfitness for trial was permanent and that it could not be accommodated by the defendant being declared a special witness.
Dr Schramm’s evidence
Dr Schramm was the first reporting psychiatrist to examine the defendant. He interviewed the defendant on 9 August 2007 and 25 October 2007 at the request of the defendant’s legal representatives. The interviews were conducted with the aid of an interpreter.
In his report of 22 November 2007, Dr Schramm reported that there was no evidence suggesting any clear psychotic thinking. He noted that, although there was strong collateral evidence of an untreated bipolar affective disorder being active for many years, there was no evidence that the offending conduct involved either manic or depressive symptoms. Dr Schramm also noted that there was evidence that the defendant was suffering from some confusional state at least in the hours/day after the events in question. Dr Schramm considered the possibility of a significant cognitive impairment such as dementia, but indicated that he had some doubts as to the defendant’s level of cooperation with formal testing. He also indicated having concerns as to whether the defendant’s amnesia for the offence was genuine, noting the defendant’s inconsistent accounts. He raised doubts as to the veracity of the defendant’s account of the offence. He indicated that this might be because the defendant was deliberately untruthful and evasive or due to genuine reasons of difficulties in recalling that time (due to the presence of a confusional state, and/or a more chronic cognitive impairment in action at the time of interview). Dr Schramm recommended further neuropsychological assessment.
Dr Schramm provided a further report dated 21 April 2008 after having been provided with Dr Keane’s report detailing her neuropsychological assessment. He noted her assessment of the defendant’s low intellectual functioning and her opinion that he was not fit for trial. Dr Schramm noted that reported statements to the prison guard by the defendant seemed to provide circumstantial evidence that the defendant was delusional at the time of the offence. Dr Schramm, however, expressed reservations as to whether the defendant was deprived of any capacity “despite considerable circumstantial evidence that this may be the case”. He referred to the variations in the history and accounts provided to him and others and noted that they “are marked by inconsistencies which are not necessarily explained by cognitive impairment alone”. He also observed that even if the defendant was impaired or deprived, the matter of intoxication “would appear to loom large here with implications for both unsoundness and diminished responsibility”. Dr Schramm considered that there was no firm evidence to suggest that the defendant was deprived of any particular capacity or of diminished responsibility.
In a further report of 2 March 2010, Dr Schramm noted two years had passed since his last interview with the defendant, but that the most recent brain SPECT study of 19 February 2010 suggested a frontotemporal type of dementia, and that the defendant was likely to have genuine cognitive difficulties that would place his ability to instruct and follow a trial in jeopardy. In oral evidence, he stated that on the basis of the SPECT scans, his view was that the defendant was permanently unfit for trial. In any event, he indicated that on that issue he would defer to Dr Wilcox.
As to the matter of deprivation or substantial impairment, Dr Schramm’s oral evidence was that notwithstanding that he accepted the diagnosis of frontotemporal dementia, and that it was likely to have been present “in some form” at the relevant time and that it would have impaired the defendant, nevertheless, he was unable to conclude, because of the state of the evidence as to the circumstances at the time, that the defendant’s mental disease had resulted in a deprivation or substantial impairment of any capacity.
Dr Fama’s evidence
Dr Fama diagnosed the defendant as suffering from mild mental retardation and frontotemporal dementia, which he noted was consistent with the results of a brain SPECT study which suggested an early to mid-stage frontotemporal type of dementia. Dr Fama considered that the condition would have been present at the time of the offences. He also agreed with Dr Schramm’s conclusion that the defendant was suffering from some form of confusional state after the murder. Dr Fama suggested that this had induced episodic states of personal confusion and disorientation, and had been associated with confabulation, leading to the implausible embellishment of events.
Dr Fama noted that the defendant offered various versions in conflict with the material in the police brief, referring to a “knife” and a “walking stick”, which seem to be non-existent, and to a “fight” for which there is no evidence. However, in Dr Fama’s view any such dispute arose only as a result of the defendant’s mental condition, which had produced confabulation.
Dr Fama was of the firm view that the defendant was deprived of the capacity to know that he ought not do the act and may also have been deprived of the capacity to control his actions.
In his report, Dr Fama also opined that at the time he saw the defendant he was fit for trial. However, in giving evidence Dr Fama stated that he had altered his view as to that matter, indicating that, in view of the nature of the defendant’s frontotemporal dementia, the better view was that the defendant was not fit for trial at the time he saw the defendant. While he had not seen the defendant since his last report, he considered that the unfitness was permanent and would have worsened given its progressive nature.
Dr Byrne’s evidence
In his report dated 2 June 2009, Dr Byrne stated that he administered the Rowland Universal Dementia Assessment Scale (RUDAS), a measure developed for use with culturally diverse and linguistically diverse people. In his report, Dr Byrne noted that:
“The history from [the defendant’s] family is consistent with a diagnosis of bipolar disorder, whereas the SPECT brain scan report is consistent with frontotemporal dementia. Frontotemporal dementia is a progressive neurological disorder that can be associated with episodes of mania and depression and in its early stages this condition is commonly misdiagnosed with bipolar disorder.”
Dr Byrne’s oral evidence was that the second SPECT scan provided convincing evidence as to a reduction in the frontal part of the brain. He was of the view that the evidence indicated that the defendant was unfit for trial and that it was of a permanent nature. That opinion was further confirmed by Dr Byrne in an additional report dated 22 April 2010, after having an opportunity to view the MRI of 10 December 2008 and SPECT scans undertaken on 6 March 2009 and 19 February 2010, in which he stated:
“... In my opinion there is unequivocal evidence of reduced tracer uptake in the frontal and temporal lobes on both of the SPECT scans. This is likely to represent reduced cerebral blood flow and reduced metabolic activity in these regions of the brain. Comparison of the scan appearance of 6 March 2009 with that of 19 February 2010 tends to suggest progression of this hypofrontal pattern. This functional pattern and the evidence of worsening over time are consistent with the clinical diagnosis of frontotemporal dementia. I thought the MRI scan was unremarkable.”
Dr Byrne did not support a defence of unsoundness of mind or diminished responsibility. He noted the defendant’s denial of having any recollection of the events in question and indicated that, since the defendant was unwilling or unable to describe his behaviour or state of mind at the time of the murder and no detailed contemporaneous reports were available, he was unable to form a clear opinion on the matter. Dr Byrne noted that the defendant had at least an insight into the alleged murder and its moral implications, given his understanding of Samoan cultural requirements of apology and reparation following the victim’s killing, which the defendant expressed in his interview. He was also unable to support diminished responsibility, although favouring an abnormality of mind and resultant impairment of capacities being present, because he could come to no concluded view as to whether there was a substantial impairment of any capacity.
Dr Byrne concluded that the defendant was not fit for trial, and that the unfitness was of a permanent nature. He opined that due to the defendant’s cognitive impairment, it was unlikely that the defendant would be able to challenge jurors, construct any form of defence, or form a proper judgment about whether to give evidence himself.
Dr Wilcox’s evidence
In his report of 29 July 2009, Dr Wilcox, a consultant neurologist, opined that the defendant suffered from frontal lobe dementia. In this respect, he referred to the clinical presentation and the SPECT scan of 6 March 2009. Dr Wilcox also provided a further report after viewing the MRI and SPECT scans, where he stated:
“With respect to the MRI head scan of 10/12/2008 in my assessment there is some very subtle and symmetrical loss of brain volume in the frontal and temporal lobes anteriorly. This suggests that some early frontotemporal dementia was possibly present at this stage. There are also several small scattered supratentorial deep white matter foci with high signal on the T2 and FLAIR sequences these probably represent small blood vessel ischemic disease and were noted in Dr Benjamin Ong’s report.
The Brain SPECT scan of 6/3/09 shows a mild-moderate defect in the anterior frontotemporal lobes consistent with mild to moderate frontotemporal dementia as suggested by the report of Dr Stanley Ngai.
The Brain SPECT scan conducted on the 19/2/2010 shows considerable progression of the frontotemporal defect and possibly spread into the left parietal lobe. The right parietal lobe and both occipital lobes are spared. Therefore I am in agreement with both the reports of Dr Stanley Ngai and the conclusion that these changes are consistent with progressive frontotemporal dementia. Dr Ngai also had access to the original scan and refers to this in his follow up report.”
In his oral evidence, Dr Wilcox explained the important role of the frontal lobe in relation to socialisation, interest, drive, organisation of motor skills and control of passions and of the temporal lobe for integration of language, memory and making association between events. He noted that the SPECT scans had shown “a moderately quick progression” of the frontotemporal dementia given the significant progression of the disease over the interval of 11 months, as shown in the second scan. Dr Wilcox thus opined that the defendant had “a relatively aggressive presentation of frontotemporal dementia”.
Dr Wilcox indicated that it was most likely that the defendant had had the dementia for months to years and that there was evidence suggestive of symptoms at the time of the offence which presage the disease, however he was unable to say to what extent the disease would have been affecting the defendant’s behaviour at the relevant time.
In oral evidence, Dr Wilcox considered the Presser criteria in relation to fitness for trial and concluded that the defendant was clearly unfit for trial and permanently so. He indicated that the defendant would have difficulties in relation to his ability to understand the nature and to follow the course of the proceedings and to understand the substantial effect of any evidence, which would worsen. The difficulty arose in part because frontotemporal dementia is associated with an apathy, even for important events, and there would also be concerns as to whether the defendant would fully recognise the importance of the events as well. There would be serious difficulties in terms of the defendant’s ability to instruct counsel due to the passivity associated with the defendant’s mental condition and his lack of interest and apathy.
Dr Morris
Dr Morris was requested by the Director of Mental Health to provide an update as to the defendant’s current fitness for trial, current treatment and recommendations for placement should a forensic order be made. He provided a report dated 19 April 2010 in which he expressed reservations as to a diagnosis of frontotemporal dementia and opined that the defendant was fit for trial.
Nevertheless, in Dr Morris’ oral evidence he accepted that he had “no doubt” that the defendant suffered from frontotemporal dementia, and that, unlike Drs Keane, Wilcox and Byrne, he was unable to offer a view in relation to fitness for trial based on any neuropsychological testing. He indicated that in that regard he would defer to the greater expertise of Dr Byrne. Dr Morris accepted the proposition put to him by Dr Varghese, that the evidence of the nature of the defendant’s decomposition when pressed on matters concerning the charged acts was consistent with a “catastrophic reaction”. He also accepted that that reaction was consistent with the defendant’s dementia.
Diagnosis
The clinical evidence presented by the experts is that the defendant has frontotemporal dementia which has been developing over some time and which was most likely present at the time of the events in question. In advising the court, Dr Varghese noted:
“The dementia [the defendant] has affects the frontal and temporal lobes and this has been demonstrated by the SPECT scan and, moreover and importantly, there is evidence of deterioration in the repeat SPECT scans. To add to the clarity of the diagnosis, the neurologist, Dr Wilcox, has demonstrated frontal lobe signs on examination in the form of emergence of so called primitive reflexes. And the dementia is also confirmed by the psychological testing and psychiatric evaluations.”
Conclusion as to the defendant’s mental condition
As to the issue of unsoundness of mind, while I am satisfied on the balance of probabilities that the mental disease from which the defendant suffers was present at the relevant times, I am unable to be satisfied to the requisite standard that that condition resulted in a deprivation of capacity.
Although Dr Fama supported a defence of unsoundness of mind and diminished responsibility, the preponderance of the expert evidence was against that view. Certainly, Drs Schramm, Byrne and Wilcox indicated in their evidence, that while it may be accepted that the defendant’s condition resulted in some impairment of his capacity to know the wrongness of the acts, the evidence as to the extent of his condition at the relevant time does not allow a sufficient degree of confidence that there was deprivation. A significant difficulty is the lack of clear evidence as to the nature or the extent of the frontotemporal dementia that was present some three years ago. An additional obstacle is that there is limited evidence as to the details of the circumstances leading to the killing of the deceased. The defendant was not able to provide an explanation. The matter is further complicated by the defendant’s tendency to confabulation that is a feature of his condition and the inconsistencies in his responses which were noted by the expert witnesses. Accordingly, I find that the defendant was not of unsound mind at the relevant times.
In relation to the charge of murder, as mentioned, Dr Fama alone of the expert witnesses supported a defence of diminished responsibility. His view, however, was favoured in the advice offered by Dr Varghese. His advice was that “the frontal lobe disorder, which is the first part of the brain to be affected by frontotemporal dementia, as against the temporal lobe, is likely to have resulted in a substantial impairment of the capacity for control”. In reaching that view, Dr Varghese was influenced by the evidence of unusual behaviour reported by the defendant’s family and others before and after the killing.
Nevertheless, Drs Schramm and Byrne were unable to support a finding of diminished responsibility, not because they were unable to conclude that there was an abnormality of mind resulting in impairment of the capacity to know, but because the evidence did not permit a concluded opinion as to whether the impairment was substantial. That was the view favoured by Dr McVie, the other assisting psychiatrist. Given the unsettled state of the evidence as to the extent of the dementia at the relevant time, it is the view that I consider ought to be preferred. Accordingly, I am unable to find that the defendant was of diminished responsibility in relation to the charge of murder.
Fitness for Trial
As Dr Varghese observed in his advice to the court, the impact of the frontotemporal dementia is quite profound. The frontal lobes are responsible for executive functioning, motivation, and being able to take on an abstract attitude, and the temporal lobes are involved in functions of memory, regulation of affect and regulation of behaviour.
Dr Schramm, Dr Keane and Dr Byrne are all in agreement that the defendant is not fit for trial. Their evidence was that the Presser criteria would not be met, particularly in terms of the ability to understand the nature of the proceedings and follow the course of the proceedings and the substantial effect of the evidence, and to instruct counsel. They highlighted problems stemming from his mental condition to do with apathy and passivity, and deficits in working memory including holding information in his consciousness and remembering data after a short period of time. The only expert who offered a reservation in respect of unfitness was Dr Morris. I was unable to place weight on his evidence, given that he indicated that he deferred to Dr Byrne’s expertise and opinion and that unlike the other reporters, Drs Keane, Wilcox and Byrne, he was unable to give any evidence based on neuropsychological testing. I note that Dr Varghese commented as follows on Dr Morris’ report:
“... reading Dr Morris’ long report buried in that is, I think, quite good evidence that there is frontal lobe dysfunction affecting behaviour. Note particularly the catastrophic reaction, which is classical evidence of dementia, the culturally inappropriate responses to the killing and the description of his general behaviour in the interview.”
As outlined, the weight of the evidence supports the finding that the defendant’s dementia renders him permanently unfit for trial. I accept that evidence, which was comprehensive and based on thorough clinical evaluations and neuro-psychological testing. Accordingly, I find that the defendant is permanently unfit for trial.
Forensic Order
A forensic order is clearly warranted in the circumstances of this case, given the very serious nature of the offences, the treatment needs of the defendant, and the need to protect the community. Those considerations require that the defendant be admitted to a high security hospital. Accordingly, I order that the defendant be detained to The Park High Security Program Authorised Mental Health Service in accordance with the submission of the Director of Mental Health. I make no approval of limited community treatment.
0
0
1