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Declarations & Statements



Under the Extradition Act 1989, the Home Secretary has, it appears, a wide but poorly-defined scope for discretion over a final decision on whether or not to extradite. Thus, the Home Secretary here takes on an explicitly judicial role and one would expect their decisions to be made so as to be as consistent as possible with the law and with the interests of justice. It is upon the shoulders of the Home Secretary to show, by example, a respect for the law.

The issue of fitness to plead has a well-established legal background, set by the case of R v Pritchard (1836), by the Criminal Procedure (Insanity) Act 1964 and by established practice. Any significant deviation from this background - on the part of the Home Secretary or any others involved in a decision on fitness to plead - should not be made lightly; to do so may amount to the abuse of justice.

In law, the criteria for unfitness to plead centre on the single question of a defendant's capacity to take part in the legal proceedings: to be able to understand what is happening to them in court, to be able to offer the essentials of a defence, and to be able to communicate satisfactorily. Chiswick (1990) quotes a defining statement of the law of fitness to plead from R v Pritchard. The jury was instructed to decide whether the accused was,

of sufficient intellect to comprehend the course of the proceedings in the trial so as to make a proper defence - to know that he might challenge any of you to whom he might object, and to comprehend the details of the evidence.[1]

In practice, this amounts to the capacity of the accused,

1. to instruct his lawyer,
2. to plead to the charge,
3. to challenge a juror,
4. to understand the evidence.

There is, essentially, no further legal definition than this, nor any more detailed clinical criteria. "'Unfitness for trial'… is a general term referring to all those factors which might render a defendant unfit to stand trial."[3]

While there may be physical reasons for being unfit for trial, this appears not to be an issue for Senator Pinochet. The medical report on his condition states thus: "Physically. Senator Pinochet would be able at the present moment to face trial…" Rather, in the opinion of the doctors who examined him, it is for mental/psychological reasons that "Senator Pinochet is not at present in a fit state to participate fully in a trial."

Therefore, what has to be determined is Senator Pinochet's mental capacity to stand trial. Chiswick reminds us, in this respect, to be clear as to the issue at hand. Legal precedent includes the "recognition that severe mental disability does not necessarily rule out the possibility of a trial. At issue throughout is the capacity of the accused to comprehend and communicate."[4] In other words, it is only evidence of mental disabilities which undermine the ability to participate satisfactorily in the court proceedings that can count towards a judgement of unfitness to stand trial.

Chiswick goes on to give us a flavour of the scale of mental incapacity which needs to be in evidence:

Usually the accused's general appearance and behaviour, his use of language and his ability to understand and answer questions will leave the interviewer in no doubt over whether he is fit to plead. Indeed, where unfitness is likely to be an issue, abnormality will probably be manifest within the first few minutes of the interview. Fitness to plead is likely to be called in question in cases where the accused… is so disordered in mood, thought processes or cognition that comprehension and communication are seriously impaired.[5]

Hence, we are talking about cases of "major mental disorder (e.g. functional psychoses, organic brain disease and mental handicap)…"[6] In Senator Pinochet's case, organic brain disease - insofar as it impinges on capacity to stand trial - appears to be the essential issue.

Again, Chiswick alerts to those carrying out such a psychiatric assessment that it is "a subjective one in which it is essential to consider the criteria described above."[7] Indeed, he cites a study on a hospital treatment programme for patients found unfit to stand trial where the focus is on instruction in court procedure. This highlights the need to direct our attention to "the specific deficits that render a defendant incompetent."[8]

What follows is a critique, from the standpoint outlined above, of the medical report on Senator Pinochet on the basis of which Home Secretary Jack Straw became "minded" to release him. This analysis was obtained by Remember-Chile from a consultant in old-age psychiatry.




The author of this comment is Master of Sciences (Oxford University), Consultant in Old Age Psychiatry in the NHS UK, and a member of the Royal College of Psychiatrists.

The author has based his comments on the full report and complementary letters published in Spanish by the newspaper El Mundo. The author assumes that this publication has accurately reproduced the reports and letters of the specialists Sir John Grimley-Evans, Dr. J. Denham, Prof. Andrew Lees and the neuropsychologist Dr. Maria A. Wyke, concerning their examination of Senator Pinochet on 5 January 2000 at Northwick Park Hospital.

According to these sources, the specialists concluded that Senator Pinochet Ugarte presents a deterioration of memory and a decrease of his intellectual capacities that leave him unfit to stand trial.

In this paper, the terms cognition or cognitive capacity are used to embrace mental functions such orientation to time, place or person, memory in its different forms, concentration, attention, language, judgement, reasoning, etc. that are fundamental to stand trial.

Factors that can affect the intellectual capacity of Senator Pinochet

Given that the inability of the patient to face a trial would be due to a loss of his cognitive abilities, it is appropriate to judge his health disorders according to the effect that they may have on that ability. The report is abundant in medical information not related to this point, and for reasons of clarity it is necessary to separate the essential from the superfluous. From this standpoint, the disorders that are present in the medical history of the patient, his present state of health and the treatments that he is receiving can be classified into four groups.

I. Pathologies unrelated to the cognitive impairment of the patient

1. Asthma, diagnosed in 1980
2. Diabetic neuropathy
3. Arthropathy of the left knee. Partial arthroscopic sinovectomy in 1996
4. Previous gout attack
5. Permanent atopic rhinitis
6. Previous operation of a left inguinal hernia
7. Decompression of the lumbar area of the spine due to stenosis of the spine and prolapse of vertebrae LA/5 L5/S1 in October 1998. Post operative ulcers due to ischial pressure
8. Multinodular goitre
9. Parkinsonian symptoms.

II. Pathologies indirectly related to a deterioration of the cognitive functions of the patient

1. "Diabetes mellitus type 2, under treatment with oral treatment." This condition, even in its non-insulin dependent form, can predispose to arterial diseases that can contribute to cause a cognitive loss. It can be accepted that it has played a role in the developing of cardiovascular disease in this patient.

2. "Defective cardiac performance identified in 1992. A pacemaker is installed and amioradone is prescribed." According to the report, it is not possible to know exactly which one is the "cardiac performance identified in 1992", nor to know whether such disorder was or is still able to induce cerebral thrombo-embolic illness, nor if its correction by pacemaker and medication has made such a complication less probable. Even then, it is appropriate to consider that this disorder may be related to the vascular illness that in turn could have contributed to cause a cognitive deficit. However, the severity of any cognitive deficit is unrelated to the severity of the defective heart function or the severity of the diabetes.

III. Pathologies directly related to the cognitive impairment of the patient

1. "Transient ischemic attacks in June 1997 and September 1999." If these attacks were caused by cerebral disorders that resulted in tissue destruction, it is possible to assume that they may have a direct relationship with the deficiency of cognitive ability. These attacks however may have no cognitive effects whatsoever, even if destruction of tissue could be demonstrated. The crucial factors determining the presence and degree of cognitive impairment in the presence of cerebral lesions are the location of the damage and the total volume of tissue lost. The report gives no information about any of these factors.

IV. Other factors that could influence the cognitive function of the patient

1. "Amioradone induced hypothyroidism. Substitutive therapy based on thyroxine." Hypothyroidism may induce transitory cognitive deficiencies (or acute confusional states), or prolonged cognitive impairment (that could simulate dementia). Replacement therapy does not necessarily prevent such manifestations, either by problems of compliance or thyroxine doses. These possibilities have not been considered by the clinicians as alternative explanations.

2. "Deafness due to acoustic trauma." Communication problems generated by severe deafness may produce frustration, anxiety, fatigue and other mental states that may reduce the efficiency of the tasks that require sufficient or intact cognition. This possibility has been ignored in the report.

3. "Prostatic symptoms of nocturia and urgency, worsening between 27 July 1999 and 5 October 1999." Prostatism could influence the mental state of the patient. Urinary retention episodes, added to associated factors to prostatic symptoms such as interrupted sleep and urinary infection may cause a loss of cognition through acute confusional states. Interrupted sleep can induced diurnal fatigue. Again, this has not been taken into account as a possible explanations for the findings in the report.

4. Pharmacological treatment. This is an issue of great importance in this case. Due to physiological factors characteristic of advanced age, medication treatment in a patient over 80 years of age has more risks and difficulties than in a younger patient. The potential for secondary and interactive effects is multiplied by the use of numerous agents.

The drugs that Senator Pinochet has to use daily are the following:
1) Budesonide
2) Metformin
3) Finasteride
4) Nimodipine
5) Allopurinol
6) Amiodarone
7) Thyroxine
8) Terazosine
9) Citalopram
10) Clopidogrel
11) Terbutaline

According to the British National Formulary, some of these drugs can individually produce effects on the mental state of patients. Some of these effects are:
1) fatigue (amioradone)
2) astenia (citalopram)
3) lack of energy (terazosine)
4) mareos (terazosine, clopidogrel)
5) vertigo (allopurinol, clopidogrel)
6) drowsiness, sopor (allopurinol, citalopram)
7) agitation, excitement (thyroxine)
8) nervous tension (terbutaline)
9) nervousness, anxiety (citalopram)
10) hypotension (nimodipine)
11) headaches (amiodarone, terbutaline, clopidogrel, citalopram)
12) amnesia, mental confusion, tendency to yawn, concentration problems (citalopram)

It is worth mentioning that citalopram can also produce alterations of taste sensation, tremor, and other motor disorders.

The probability of side effects, particularly those affecting mental state, is increased when eleven different drugs have to be used on an octogenarian patient. Apart from specific risks that each drug presents when considered individually, there are the risks resultant from interaction and potentiation between them. These effects may manifest themselves in disorders of mental state, including transitory or prolonged cognitive impairment.

The factors mentioned above may have played a role in or been the cause of the various transient episodes suffered by the patient in the recent past. They could also crucially have influenced the cognitive tests carried out on 5th January 2000, but have not been considered by the clinicians signing the report.

Results of clinical and laboratory examinations

Many of the present and past clinical investigations and examinations mentioned in the report do not have abnormal results and are irrelevant to the issue of fitness to stand trial.

Those that show abnormalities may be placed in three groups according to the influence that they could have in the mental state of the patient.

I. Clinical and laboratory findings that reveal abnormalities unrelated to the patient's cognitive functions

- Minor non-specific component theta on EEG.

- 120 ml residual bladder volume.

- Symptoms suffered after surgical vertebral decompression in 1998.

- Recent walking difficulties and insensibility of the feet soles.

- Difficulties resulting from parkinsonism, urinary problems, somatic pains, loss of manual dexterity, etc.

The majority of the abnormalities found in the physical examination are equally irrelevant to the evaluation of the cognitive ability of this patient. The neurological examination is normal for the majority of its sections. Positive findings are unrelated with the mental state of the patient. It is worth mentioning, for reasons that will become clear later, that the existence of primary reflexes was noted, reflex of grimace present and palmomental lateral positive more to the left than to the right.

II. Clinical and laboratory investigations revealing abnormalities that might indirectly relate to the patient's cognitive functions

- Doppler studies of carotid and vertebrae show atheroma. Apparently this factor is not clinically significant for the team of clinicians.

- "Pronounced deafness, but the patient is capable of keeping a conversation with his hearing aid on." Deafness can be an obstacle to participate in a trial, but this patient can communicate satisfactorily. Therefore this factor is not relevant to the issue of fitness to stand trial.

III. Clinical findings that directly might relate to the patient's cognitive function

- "CT scan consistent with small ischaemic lesions; there is also some ventricular enlargement and minor atrophy, consistent with a slight primary degenerative deterioration."
It can be commented that the ischaemic lesions are not described in terms of location, but they are small, and their clinical significance is uncertain. The radiologist reported that both ventricular enlargement and minor atrophy were consistent with a "primary degenerative" condition, i.e. dementia. Wisely, the clinicians disregarded this suggestion no doubt because it is well known that many cognitively normal people in this age group show the same changes. The diagnosis of dementia in any of its forms and severity is not based on brain imaging or psychometric testing. It is a clinical diagnosis normally carried out in the U.K. by psychiatrists specialised in Old Age Psychiatry, with the help of a multidisciplinary team.

- "10 months of worsening memory, recently more accentuated, with occasional difficulties in remembering names of persons, dates and remote events. Transitory events with failure to recognise persons, convert ideas into speech or become aware of immediate situations."

- "One event of blurred vision, another of circumlocution, nominal dysphasia, frontal tremor, inexpressive face, poor reflexes and jaw spasms." This patient's own doctors have described them as "Cerebral events of ischaemic character" and made a "clinical diagnosis of multiple small bilateral cerebral infarctions".
It is not certain that all these events are cerebro-vascular in character. Explanations suggested above (see "IV. Other factors that could influence the cognitive functions of the patient") could explain some of them.
The period of ten months is brief for dementia. This relative short evolution of Senator Pinochet's mental condition is consistent with the mild impairment found by the team in the Mini Mental State Examination (score 23/30).

- Depression during summer 1999; loss of interest in activities that were undertaken before. Apparently, this is no longer so. The patient was alert and co-operative, with no evidence of depressive symptoms, although he tired easily.

- "Cerebration. The patient showed slowness in comprehension and difficulties in understanding complex instructions. Bradiphrenia and circumlocutory speech were found but not dysphasia of lower levels."
There is no further comment on these symptoms, which are described in general terms. When the clinicians used the quantitative cognitive test Mini Mental State Examination, the results are at odds with these findings. A tired physically frail elderly individual may appear mentally slow.

- CT scan of the basilar artery of the brain. "Generalised moderate atrophy with evidence of lacunar infarctions. No significant changes since previous scan." There are no dates available for this and the previous scan, but they may have been taken during the last few months. The absence of significant changes between these scans indicates absence of detectable progression of the vascular damage.

- Intelligence tests
1. Wechler: Numeric: 75; Vocabulary: 125; Similarities: 110; Geometrical drawing: 75
2. Progressive matrixes: 100
Both intelligence tests indicate that Senator Pinochet exhibits presently a level of intelligence within the normal range. A normal intelligence is enough to stand trial. The fact that the current level might be lower than the one he may have enjoyed in the past is not relevant with the issue in question.

- Memory test:
1. Drawings:12/20
2. Brief story: 1/16
3. Objects: 3/12
Memory after 30 minutes: Drawings: 6/12; Story: 0; Objects: 6/12
These results, particularly memory after 30 minutes is the worse performance the patient had in the day of the exam. This is inconsistent with the other cognitive tests and should be re-tested. To accept as valid a test carried out after long hours of clinical examinations seems inappropriate, as will be discussed later.

Criticism of the conclusions of the specialists who examined Senator Pinochet

The conclusions reached by the medical team who examined Senator Pinochet were included in the letter of 6 January 2000, signed by J. Grimley-Evans, M.J. Denham and A.J. Lees. Those conclusions will be examined here in the order in which they appear in the letter.

While there is no doubt of the existence of cerebral lesions likely to have been caused by vascular illness, there is no sufficient basis to indicate that those lesions are progressive. Certainly, there is no anatomical evidence of progression if the imaging studies of this patient are considered. It seems clear, from the report, that the cerebral scan which reveals lacunar infarctions does not show variation with respect to the previous scan, and from that point of view the lesions are stationary. The purely clinical evaluation of progression in vascular cerebral damage is not reliable. This patient has presented transitory episodes compatible with ischaemia and infarctions from which he has clinically recovered.

The 10 months' period that the specialists assign to the evolution of the disorder is too short to evaluate the progression of an illness that may have evolved over several years. Furthermore, by its own nature, the most likely disorder affecting this patient, i.e. a multi-infarct mild damage of the brain, is characterised by fluctuations in the intensity of its clinical manifestations.

Furthermore, the report does not offer any comment about the differential diagnosis of these episodes. Undesired side effects on a patient subjected to simultaneous treatment with drugs that might cause hypotension and effects on mental state, either individually or simultaneously, offer an explanation that should not simply be ignored. Equally, concomitant pathology (see "IV. Other factors that could influence the cognitive function of the patient") should also be considered in this respect.

Further on, the report says that there are critical tests that would prove extensive cerebral damage. For example, "damage in the pyramidal zone, which produces spasms on the basal glanglia" is mentioned, which in turn produces Parkinson's syndrome. Even though it may not have been the intention of the authors of the report, the impression is created that the symptoms of Parkinson's disease, a "disorder of movement", is associated with a unitary cause of extensive cerebral damage.

The truth is that the presence of these symptoms is not an unequivocal sign of organic brain damage, and the causes of Parkinsonism are multiple.[1] Furthermore, "it is difficult to establish a causal relationship (with Parkinsonism) to arterial cerebral illness, when it exists. Both disorders may occur simultaneously purely by coincidence".[2]

Another supposedly critical proof of the existence of cerebral damage of the frontal lobes constitutes, according to the report, the presence of "primitive reflexes". Again, it should be stated that these reflexes are not in the least an unequivocal manifestation of frontal damage, since they are present both in patients with organic cerebral damage, and in patients who suffer mental illnesses without brain damage.[3] These reflexes have also been found in 20% of normal people of 30 and 40 years of age, and on a third of those aged 60 or more. Furthermore, the incidence of these reflexes in the normal population increases with age.[4]

The specialists have demonstrated the existence of some memory impairment in this patient, something that will not be disputed here. However, the interpretation of the results merits a more detailed analysis (see below), since the evaluation of their degree and significance made in the report appears inappropriate.

The report states that a major part of the ailments is attributed to the zones irrigated by the basilar artery. However, there is no mention of appropriate examinations made to evaluate the functional and anatomical state of this artery. The only evidence mentioned is the presence of signs of calcification in that vessel, as shown in a CT scan. Although there has not been time to find the references to refute this assertion in a erudite way, it is a well known clinical fact that calcification of an artery is frequently of no clinical significance, and that calcification of the basilar artery is not infrequently a fortuitous finding. In this part of their conclusions the authors of the report present as demonstrated, without further proof, the existence of frontal lobe damage, something this comment has refuted. More serious for the credibility of their report, they treat the unsubstantiated presence of frontal lobe damage as an indication of a more generalised arterial illness in the brain.

Finally, we shall focus on the reasons why it is considered that Senator Pinochet is not fit to stand trial.

The report states that one of the reasons for unfitness to stand trial is the memory impairment for remote and recent events. It is interesting to notice that the three clinicians who examined the patient during the morning session found only a mild impairment of mental abilities. They examined the patient using a 30-item test called Mini Mental State Examination. This test was introduced by Folstein in 1975, and has gained enduring popularity among both clinicians and researchers. Is spite of its relative brevity, it allows us to evaluate orientation, memory, attention, concentration, ability to name objects, ability to follow written and verbal orders, write a sentence and copy a geometrical figure. The maximum score is 30, while scores of less than 24 are usually indicative of cognitive impairment. This patient scored 23, which suggests either a mild cognitive impairment or an absence of such impairment. The report fails to give the items in which the senator failed.

This test is widely used by psychogeriatricians as a screening tool to diagnose dementia, since it covers the main brain cognitive functions that may fail in the dementias. The Wechler's test used by Dr. Wyke is a more limited instrument since its main purpose is to measure intelligence, and for that reason it is not used to diagnose dementia. The fact that the patient showed an intelligence quotient within the normal range is indicative of his mental ability to stand trial, rather than the opposite. The fact that some aspects of the results suggest a loss in comparison with previous levels of intellectual functioning in not in itself diagnostic of a dementia, nor relevant to the ability to stand trial.

The result 23/30 would indicate the possibility of a mild dementia, and no psychiatrist would jump into the conclusion that there is a case of definitive dementia. Normally, this diagnosis is made after clinical, psychological and social evaluations carried out for an appropriate period, and even then only after having excluded any possible concomitant condition capable of producing a cognitive impairment. The assessment of severity was apparently done using the poor results of the memory tests carried out during the afternoon, ignoring the results of the Mini Mental State Examination on that morning.

The results of the morning contradict the poor performance of the afternoon under Dr. Wyke. Far from trying to find an explanation of this important discrepancy, the clinicians limited themselves to adding Dr. Wyke's conclusions to their report. Several solutions for this problem exist; the main ones are related to the proneness to fatigue of this patient, and the actions of the drugs, both therapeutic and unwanted. It is interesting to see that even during the afternoon session, there were variations in performance. For example, the memory failure reported in the formal tests passed is inconsistent with the initial adequate memory for facts and dates of the past that the patient showed at the beginning of the session. The omission of any attempt to discuss these issues between the examiners is another serious weakness of their report.

The report states that a limited ability to understand complex sentences and questions due to memory and impaired processing of verbal information would incapacitate the patient to stand trial. However, this ability appears impaired only in the afternoon, and partially so. It is evident that the patient, provided he had appropriate explanations and repeated instructions, was able to follow instructions and adequately co-operate with tests and examinations. Quite strikingly, complete incapacity to understand instructions was demonstrated only in the afternoon session, after many hours of interaction with different examiners and witnesses. A state of fatigue and transient mild confusion could explain the discrepancy.

The reduction in the patient's ability to express himself audibly, understandably and coherently is, for the specialists, yet another factor impeding him to stand trial. However, the very fact that the three clinicians in the morning and Dr Wyke in the afternoon successfully completed their prolonged assessments is a demonstration that this reduction is insufficient to impair a satisfactory level of communication. Besides, throughout the report there are several allusions to the ability of the patient to understand, respond, co-operate, etc. leading us to conclude that perhaps too much weight was given to the impairment of certain cognitive abilities that were evident only in the afternoon.

Finally, fatigability would affect he patient's ability to stand trial. Obviously, such a tendency exists by reasons of age, physical illnesses, mild cognitive impairment and the effects of drugs. However, this factor is not a legal impediment to stand trial.

The specialist team reiterates their conviction that the impairments that they identified are due to brain damage, are consistent with the symptoms and are homogeneous in presentation. This author has already noted the conspicuous absence in this report of any consideration of alternative clinical explanations. The reader is invited to consider the defective foundations of the so-called "extensive brain damage".

The comment that a trial would produce stress that would accelerate the vascular disorder is too hypothetical a matter to deserve a comment. This point does not help us to understand the prognosis, nor is relevant to the medico-legal issues regarding ability to stand trial.

Final comment

The recommendation that Senator Pinochet is not fit to stand trial is at odds with the available evidence.

Dr Enrique Zapata
Consultant Psychiatrist & Medical Director
Milton Keynes Community NHS Trust
Hospital Campus
Milton Keynes

- Legal introduction
1. Chiswick, Derek, Fitness to stand trial and plead, mutism and deafness, p.172, in Bluglass, Robert and Bowden, Paul (ed.), Principles and Practice of Forensic Psychiatry, London: Churchill Livingstone, 1990, pp.171-177.
2. Ibid., p.174.
3. Ibid., p.172.
4. Ibid., p.174.
5. Ibid. (Our emphasis.)
6. Ibid.
7. Ibid. (Our emphasis.)
8. Ibid. (Our emphasis.)
- Medical commentary
1. Eadie & Sutherland (1964) J Neurol Neurosurg & Psychiatry 27, 237-240; Pallis (1971) BMJ, 3, 683-690.
2. Lishman, WA (1998) Organic Psychiatry. 3rd Ed. Blackwell Science.
3. Keshavan et al (1979) Ind J of Psych 21, 267-270.
4. Jacobs & Grossman (1980) Neurology 30, 184-188.

[Minor revisions made, 19.3.00, to original document of 20.2.00]

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