THE SOCIAL SECURITY COMMISSIONERS

Commissioner’s Case No:  CSI/146/03

SOCIAL SECURITY ACT 1998

APPEAL FROM THE APPEAL TRIBUNAL UPON A QUESTION OF LAW

COMMISSIONER:  L T PARKER

Oral Hearing

Appellant:  				          Respondent:  Secretary of State

Tribunal:  Dumfries			          Tribunal Case No:  

DECISION OF SOCIAL SECURITY COMMISSIONER

1.	The decision of the appeal tribunal sitting in Dumfries on 8 November 2002 (the second tribunal) is in error of law.  I therefore set it aside.  However, as invited so to do by the Secretary of State and using my powers under s.14(8)(a)(ii) of the Social Security Act 1998, I substitute my own decision in the case which is to the same effect as that of the second tribunal.

2.	This is as follows:-

The claimant’s appeal is dismissed.  The Secretary of State’s decision dated 3 May 2000 is confirmed as correct.  The claimant suffers from acromegaly.  However, the claimant has not demonstrated on a balance of probabilities that that condition was caused in any way, nor aggravated by, an accident accepted as arising out of and in the course of his employment which occurred on 13 February 1974 (the relevant accident).  Accordingly, the claimant is not entitled to disablement benefit as he has no loss of physical or mental faculty from 29 May 1974 resulting from the relevant accident.

Background

3.	The claimant’s date of birth is 10 November 1947.  He spent much of his working life as a detective and special branch officer in the London Metropolitan Police.  On 13 February 1974, when working as a police constable, he received a punch to the left side of his head from a large and powerfully built man who was psychiatrically disturbed.  Although the claimant then fell back against the wall, he was able subsequently to draw his truncheon and attempt to hit his assailant.

4.	On return to the police station he was seen by the police surgeon who pronounced him fit for duty.  His first recorded absence from work after the relevant accident is from 1st September 1976 for influenza.

5.	In a statement signed 20 February 2000, made to a doctor (the medical adviser) examining him on behalf of the Secretary of State, the appellant states that he had headaches in the area of the injury received in the relevant accident for months afterwards but they settled down.  He also developed problems with his eyesight, but these too settled some twelve to eighteen months after the accident.  At about the same time, he suffered a collapse at work.  Then in 1976 he began to experience tremendous pressure to his forehead and to the bridge of his nose, which continued.  Other unpleasant symptoms gradually developed.

6.	A similar history is given in his “patient’s story”, which was apparently published on the internet and a copy of which appears in the papers.  He was invalided from the police on 31 December 1984 but it was not until March 1989 that his diagnosis as one of acromegaly was confirmed.  A tumour was removed from his pituitary gland on 21 August 1989.  However, he regards his condition as having worsened since then.  He has attended Professor Besser, director of medicine and endocrinology at St Bartholomew’s Hospital in London.

7.	On 6 January 2000, the appellant claimed disablement benefit in connection with the relevant accident.  This was refused following the medical adviser’s (MA’s) advice that the relevant accident had caused a soft tissue injury to the head but there was no loss of physical or mental faculty therefrom from 29 May 1974.  The MA’s opinion was to this effect:-

	“Acromegaly is caused by an over active pituitary gland producing excess growth hormone.  This is not a consequence of head injury – (this is the opposite of hypo pituitarism).”

The tribunal history

8.	The claimant appealed to an appeal tribunal on 18 May 2000.  Significantly, his appeal includes the following passage:-

	“The best minds in the world cannot say what causes a pituitary tumour but I have spoken with the top Professors in the country and in as much as they cannot say a blow to the head certainly causes acromegaly then they likewise have not ruled it out…”

9.	A tribunal sat to hear his appeal on 15 January 2001 (the first tribunal).  The appellant lodged various documents about pituitary dysfunction.  The medical member of the first tribunal introduced himself as an endocrinologist.  The appellant told the first tribunal that he had been last assessed by Professor Besser two years previously.  He said that he had not asked Professor Besser’s opinion as to the causation of his acromegaly.  

10.	The appellant produced three photographs for the first tribunal.  They were taken in 1968, 1976 and 1977.  It has been part of the appellant’s case that Professor Besser’s team saw no hint of acromegaly in the 1968 photograph but considered that the 1976 photograph showed the first signs of acromegaly and that of 1977 “full blown” acromegaly.  The last sentence of the record of proceedings of the first tribunal however states:-

		“Find 1968 photo shows signs of early acromegaly”.

11.	The first tribunal, having noted in its findings that its medical member had in his professional life dealt with many hundreds of acromegalics, disallowed the appeal:-

	“…the Tribunal found on the balance of probability that the injury which the appellant suffered in 1974 was not the cause of the appellant’s acromegaly.  The Tribunal had regard to the copious information provided by the appellant which was considered by the Tribunal.  However, the same in the tribunal’s view did not lead it to conclude on the balance of probability that the link existed in the instant appeal between the soft tissue injury and the onset of acromegaly.  The tribunal also had regard to the Medical Services advice minute of 28.12.00. the (sic) Tribunal adopt in its entirety the reasoning therein.”

12.	Appeal was made to the Commissioner on the grounds of a breach of the rules of natural justice, because the minute of 28 December 2000 referred to had not been in the appeal papers available to the appellant.  It was also argued that the first tribunal should have considered and recorded whether the relevant accident aggravated any pre-existing condition.

13.	The Secretary of State, in a submission dated 4 July 2002, supported the appeal taken against the first tribunal’s decision.  It was agreed that the relevant minute should have been made available to the appellant and that, although it had not been argued that the relevant accident aggravated the claimant’s condition, it might have been reasonable for the first tribunal to consider this issue.  The submission of 4 July 2002 concluded:-

	“This is a far from straightforward case and I respectfully suggest that the Commissioner should direct that the new tribunal should include both an endocrinologist to consider the acromegaly and an oncologist to consider the possible cause of the pituitary tumour.  I also suggest that the tribunal should obtain a report from Professor Besser….”.

14.	In CSI/92/02, the Commissioner set aside the decision of the first tribunal, with no reasons and only one direction:-

	“The fresh tribunal will note the content of the Secretary of State’s submission.”

15.	When the appeal came before a second tribunal, the missing advice minute from medical services was in the papers.  This states:-

	“Nowhere can I find any conclusive evidence that tumour or genetic mutation of a previously inactive tumour is on the balance of probability caused by heavy injury.”

16.	The appellant was again present and represented at the second tribunal hearing.  However, whereas his representative previously had been a welfare rights officer, from the second tribunal hearing and continuing he has been represented by Mr Colin Moore of the Police Federation.  Further information from the claimant was produced for the second tribunal, mainly reports of medical studies taken from the internet.  A presenting officer on behalf of the Department was also at the hearing.

17.	At its commencement, the chairman raised with the parties the point that the medical member of the tribunal was neither an endocrinologist nor an oncologist.  Mr Moore submitted that the tribunal and the appellant would be disadvantaged.  He further submitted that as no report had been obtained from Professor Besser, he wished to have an adjournment to obtain an expert report.  He said he believed he could get funding for such a report.  The presenting officer said that the Secretary of State considered that the medical member on the panel was qualified to deal with the matter if he was happy to do so.

18.	The second tribunal recessed to consider the preliminary issue.  It then decided to continue because, as it subsequently put in its statement of reasons:-

	“It was noted that the presenting officer was not upholding the request in the submission to the Commissioner, in the tribunal’s view the appellant has had more than adequate time to obtain any report.  There is a large volume of information contained within the papers already supplied by the appellant.  In the view of the tribunal the appeal should proceed today on the basis of the information available to it.  If at the end of the hearing the tribunal considered further evidence was required, they would be able to adjourn to obtain same.  It was further the view of the tribunal that [the current medical member] has been appointed as a medical member suitably qualified to sit on a medical appeal tribunal.  A consultant endocrinologist sat on the last tribunal and the Appeals Service have been unable to identify any other oncologist or endocrinologist as being a panel member available to sit.  The tribunal considered that they should continue with the hearing on the basis of the tribunal as constituted today”.

19.	The second tribunal, like the first, disallowed the appeal:-

	“The tribunal find on the balance of probability that the injury which the appellant suffered on 13.2.74 was not the cause of the appellant’s Acromegaly either by causing a pituitary tumour de novo or by causing mutation of a pre-existing inactive pituitary adenoma.”

20.	In its reasoning, the second tribunal said that the appellant required:-

	“…to prove on the balance of probabilities that the blow to his head either caused a pituitary tumour or caused mutation of a pre-existing inactive adenoma of the pituitary gland.”

21.	The second tribunal reviewed the “considerable volume of information” before it but noted that most of the cases were “anecdotal single cases only” and concluded:-

	“The tribunal did not consider any further evidence was necessary for the proper determination of this case.

	In the tribunal’s view there is no persuasive evidence that a blow to the head either causes an adenoma of the pituitary gland or would cause a mutation of a pre-existing inactive pituitary adenoma.  On the balance of probability therefore the tribunal find that the accident sustained by [the appellant] on 13.2.74 did not lead to his present condition of Acromegaly and the appeal is accordingly refused.  The Secretary of State’s decision is upheld in full.”

Appeal to the Commissioner

22.	Appeal by the claimant against the decision of the second tribunal is made on several grounds with which I shall deal in my own decision.  The appeal is supported by the Secretary of State on one ground only.  This is that if the tribunal considered it inappropriate to obtain a report from Professor Besser or an alternative expert report, then the opportunity should have been given to the claimant to obtain one.  The Secretary of State’s first written submission states:-

	“….the Commissioner’s direction gives the impression that the tribunal would obtain the report.  In my view, the claimant cannot be criticised for expecting this to be the case and therefore not obtaining the report himself.  I submit that in refusing to adjourn, the tribunal have breached the rules of natural justice and have thereby erred in law.”

23.	Another Commissioner granted leave but I have, by directions, raised various questions about an appeal tribunal’s powers to obtain assistance from an expert.  In addition to further written submissions on this point by the Secretary of State, those matters were addressed at the oral hearing before me.

24.	Prior to that oral hearing, both parties produced further medical evidence.

25.	On the appellant’s behalf, there is lodged a report dated 31 July 2003 by Dr Robin S Howard, a consultant neurologist at the Department of Neurology at St Thomas’ Hospital in London. 

26.	In Dr Howard’s report, he records meeting the appellant and then sets out the history.  There is no indication of any clinical examination.  He refers to the diagnosis of acromegaly and its distressing symptoms in the appellant’s case, none of which is in dispute.  

27.	The important part of his short report is in the final two paragraphs which read:-

	“In my view there can be absolutely no doubt that this gentleman has acromegaly and that the symptoms were manifest in the early 1980’s (sic).  I think that it is quite possible that some of the psychiatric disturbances, which were present in the late 1970’s (sic), could also be attributed to the acromegaly.

	It is also quite clear that pituitary dysfunction may occur as a consequence of head injury.  The neurological literature is very clear on this point and it is well known that the pituitary stalk may be damaged following head trauma.  The relationship of head trauma to acromegaly is a little less certain but there are a number of very clear reports indicating a temporal association between a head injury and the development of acromegaly.  I think that there can be no doubt that in [the claimant’s] case there was a clear temporal relationship between the head injury and the development of the acromegaly.”

28.	The Secretary of State has produced a report dated 6 October 2003 from Dr Susan Reed, a doctor in the Department’s Medical Services.  Her report takes the following form.  First of all, she explains the anatomy, physiology and pathological processes relevant to the case.  Then before she reviews the evidence produced by the appellant, she says:-

	“A thorough search of both textbooks and the internet has failed to link hyperpituitarism, and in particular Acromegaly, with head trauma, either as a direct cause of it or as having an exacerbating effect.  However a severe head injury can cause hypopituitarism, but this is an entirely different condition to Acromegaly.”

29.	Her views on Dr Howard’s letter are these:-

	“Dr Howard is a neurologist, and hence not an expert in endocrinology.  His expertise is in the central nervous system not the endocrine system.  His views expressed in the final sentence are not within the consensus of medical opinion and are outwith the accepted views on pituitary function.  The presence of one or two papers which may suggest a link would not be accepted as changing the consensus view, based on years of experience and research, that trauma does not cause Acromegaly.

Trauma to the pituitary stalk leads to hypopituitarism, and most commonly to the posterior pituitary, causing it to under-function.  Thus the common presentation is diabetes insipidus. ….

The blood supply to the anterior pituitary passes alongside the pituitary stalk.  If this is damaged it leads to under-functioning of the anterior pituitary because the pituitary cells are starved of nutrients and therefore cannot produce hormones, whereas Acromegaly is due to cells increasing the production of hormones.

…….

Acromegaly is a distressing condition.  As with other conditions, which have an insidious onset, patients often relate the onset to an acute event, which has no relation to the cause.  Often this is because the acute event has drawn attention to the accumulated effects that have occurred but have gone unnoticed because each in themselves was minor and of very slow progression.  For example in Acromegaly the shoe size is very gradual but may be noticed when purchasing a particular form of footwear, and related to a trip a few days previously.  It is the nature of humans to find a cause and often that “cause” is not the actual cause, but the event which drew attention to the condition.

There is no doubt that [the claimant] has Acromegaly, and has suffered greatly from the effects.  However the vast majority of evidence on the condition does not support the view that head trauma causes or exacerbates or aggravates Acromegaly.”

The oral hearing

30.	The case came before me for an oral hearing on Thursday 4 December 2003 at the request of the appellant.  As already noted, he was represented by Mr Colin Moore of the Metropolitan Police Federation.  The Secretary of State was represented by Mr Brown, Solicitor, of the Office of the Solicitor to the Advocate General.  I am indebted to them both for their assistance.

31.	The appellant gave evidence and acted throughout with dignity and candour.  Unfortunately, he has a very distressing condition.  Undoubtedly, he genuinely believes that it was triggered by the relevant accident.  He has diligently researched the internet.  He works hard for various organisations associated with pituitary dysfunction.  The issue for me however is whether the second tribunal erred in law and, if yes, is there sufficient evidence on which to base my own decision?

Arguments for the appellant

32.	Mr Moore argues that acromegaly is a unique disease and it was crucial that there was expert evidence available to the second tribunal.  The Commissioner’s guidelines were not followed.  The second tribunal breached natural justice by failing to adjourn at the appellant’s request.

33.	There is nothing to indicate that the appellant’s acromegaly is genetic.  He was in previous good health.  Soon after the relevant accident, a severe punch, his health started to deteriorate.  Dr Howard’s report underscores the clear temporal relationship in the appellant’s case between the head injury and the development of the acromegaly.  What Dr Howard is actually saying is that there is, on a balance of probabilities, a causal link in the appellant’s case between the relevant accident and the development of his current condition.  That is the conclusion of an expert in this rare disease.

34.	The conclusions of the second tribunal were unsafe because there was no such expert in the field at the hearing nor was any report by an expert in acromegaly available to the second tribunal.

35.	Mr Moore’s final submission was put in the following way; 22.4 per cent of the population has a non-functioning pituitary tumour.  Only in a small number of those is there mutation resulting in acromegaly.  Factors causing such mutation can be physical or emotional stress or interruption of the blood supply.

36.	I invited the appellant to point to any particular evidence on which he relied to show the essential causal link.  He singled out his own “patient’s story”, already referred to, and what he has throughout called the “Baxter” paper.  With hindsight, he knows that head injury played a part in his acromegaly.  Every doctor he has seen has asked him whether he has had a head injury and patients using the pituitary dysfunction helpline report a similar mode of questioning in their own cases.

Arguments on behalf of the Secretary of State

37.	Mr Brown contends that, albeit the previous Commissioner only laid down guidelines, it was reasonable for the appellant to expect the second tribunal to obtain an expert report.  He agrees that they were in breach of the rules of natural justice not to have so done.  However, in no other respect does Mr Brown consider that the tribunal erred in law.

38.	So far as the composition of a tribunal is concerned, the Secretary of State now submits that it is for the tribunal to determine its own composition, subject only to the restraints of regulation 36 of the Social Security and Child Support (Decisions and Appeals) Regulations 1999 (the regulations), which requires one or two medically qualified panel members in an industrial injuries case.  Some specialists are in short supply.  The consultant medical member of the tribunal (as here) is experienced in assessing the reports of other experts and can decide how far, if at all, input is required from another expert.  In this case, the issue was one of assessing written material about the causes of acromegaly (as the diagnosis is not in dispute) which requires no particular type of expertise in making an appropriate analysis and evaluation.  Under s.94 of the Social Security Contributions and Benefits Act 1992, the onus of proof lies on the claimant to demonstrate the necessary causal link.

39.	The Secretary of State does not support the other written grounds of appeal.  Evaluation of the evidence and determination of the merits is for a tribunal and the second tribunal expressly considered whether or not the relevant accident had aggravated a pre-existing condition.  Furthermore, no argument was ever put that a psychological condition, in some way discrete from the effects of acromegaly, was linked to the relevant accident.  Finally, the tribunal was not required to identify an alternative cause for the appellant’s undoubted acromegaly.  The second tribunal’s role was to determine on a balance of probabilities whether the appellant had discharged the onus of showing a causal link between the relevant accident and a loss of faculty and had no wider remit on causation.

40.	In response to my queries about how a tribunal could seek assistance, it was Mr Brown’s submission that the Social Security Act 1998 had widened the relevant powers of tribunals when compared with those given by sections in the Social Security Administration Act 1992 which have been repealed.

41.	S.53 of the Social Security Administration Act 1992 allowed a tribunal to refer “any question of special difficulty” to an expert for examination and report.  Although that has gone, s.20 of the Social Security Act 1998 gives a power to all tribunals which was formerly given by s.55 of the Social Security Administration Act 1992 only to disability appeal tribunals.  Section 20 allows the legally qualified panel member to refer a claimant for examination and report to any medical practitioner.  There is no limitation to an expert.  Furthermore, under s.7 of the Social Security Act 1998 and regulation 50 of the regulations, a member of the tribunal panel may assist the tribunal as an expert witness.  However, the provision for an expert to sit as an assessor (under s.56 of the Social Security Administration Act 1992) has been repealed for tribunals, although not for Commissioners.

42.	A tribunal has a general power under regulation 43 of the regulations to summon witnesses, but Mr Brown accepts that there is no sanction to enforce it.  Under regulation 38, the legally qualified panel member has a wide power to make directions, which encompass a direction to produce a particular kind of report.  The only possible sanction for a failure by a party to comply is striking out the appeal by a tribunal or its drawing an adverse inference from the omission, although neither course of action is either mandatory or necessarily appropriate.

43.	However, in this particular case, Mr Brown suggests that no further report is necessary.   Both the first and second tribunals considered that they had sufficient medical evidence on which to reach a proper conclusion.  Additional medical evidence is now available to the Commissioner.  Even if a report from Professor Besser had been obtained and it fully supported the appellant’s proposition with respect to causation (and there is no indication that would happen) the evidence already in the papers more than outweighs any contrary opinion if such were produced.

44.	Mr Brown therefore strongly urges that I substitute my own decision and that it must on the evidence be one adverse to the appellant.  Dr Howard’s report posits no more than a possible temporal relationship between a head injury and the development of acromegaly.  All that he is saying is “well known” is that the pituitary stalk may be damaged following head trauma but this, as Dr Reed’s report shows, has different results from those in issue.  Dr Reed’s review of the papers is extensive.  She sets out the consensus of medical opinion which, Mr Brown submits, is that there is no known link between hyperpituitarism and head trauma.  It is accepted that there is one with hypopituitarism but this is the very opposite of acromegaly, the appellant’s condition.

45.	Mr Brown says that Dr Reed’s qualifications have been criticised on behalf of the appellant on the basis that she is the equivalent of a general practitioner and therefore not qualified to make any judgement when contrasted with an expert such as Dr Howard.  Mr Brown submits however that, unlike a general practitioner whose primary role is one of diagnosis and treatment, Dr Reed is a specialist in Disability Assessment medicine (she has the relevant diploma and is also an examiner for that diploma).  Her expertise is in assessing how a person is affected by disease or disability, which typically includes issues of causation and relevance.  Another postgraduate qualification she has is in occupational medicine.  Mr Brown contends that Dr Reed is thus well qualified with respect to her conclusions.  

46.	Moreover, the endocrinologist who sat on the first tribunal was of the opinion (as recorded) that the appellant was showing signs of early acromegaly in 1968 i.e. before the relevant accident.  But the most important consideration is that both the first and the second tribunals decided as they did because the copious documentation supplied did not lead either such tribunal to conclude that the necessary link had been shown between the relevant accident and the onset of acromegaly.  Neither tribunal considered that it required any further information.  Mr Brown submits that the evidence overwhelmingly shows that, on a balance of probabilities, the relevant accident on 13 February 1974 did not lead to acromegaly either by way of direct causation or by aggravation of an existing condition.

My conclusion and reasons

Composition of the tribunal

47.	The second tribunal did not contravene any Commissioner’s direction in sitting without an oncologist or endocrinologist because all the Commissioner required it to do was to take note of the earlier recommendations by the Secretary of State.  Furthermore, as a practical matter, there were no such specialists as panel members other than one who had already sat in the same case and was therefore barred from sitting again.

48.	It is for the President of the Appeals Service to select members of the appeal tribunal in a particular case and the pool is inevitably limited to those on the appointed membership panel.  Even if a case is unusual, a medical member on the tribunal will ordinarily be able to deal adequately with competing medical views.  I do not consider the tribunal erred in law in failing to ensure that it had particular specialists sitting on the tribunal.  For a similar reason, exercising the discretion conferred by section 7(4) of the Social Security Act 1998 would have been pointless; just as there was no panel member of the appropriate specialisation to sit as a member, there was no such specialist to appear as a witness.

Powers of a tribunal to obtain assistance

49.	Unlike Mr Brown it is my opinion that, in important respects, the powers of a tribunal have been restricted by the 1998 changes.  The definition of “expert” under s.53 of the Social Security Administration Act 1992 was drawn very widely indeed.  Section 20 of the Social Security Act 1998 may not be restricted to “experts” but a tribunal acting under s.53 always considered it could classify a general practitioner or an examining medical practitioner as an expert under this section.  Therefore, the powers available to a disability appeal tribunal under s.55 could be exercised by a medical appeal tribunal acting under section 53. 

50.	Section 20 of the Social Security Act 1998 is not as useful to a tribunal as the former s.53.  This is because the latter was not restricted to medical examinations and reports.  If, for example, difficult issues arose in a prescribed disease case about the nature of a tool or an engine, or a type of oil rig, these could be referred to an engineer.  Section 7 of the Social Security Act 1998 has introduced expert witnesses; but as such expert witnesses must be members of the panel their expertise can only be as either medically qualified, or having a disability qualification or financially qualified.  Moreover, tribunals are naturally reluctant to exercise their power under s.7 and regulation 50 to use an expert panel member witness for any purpose other than to provide a written report.  This is because if such a member attends a hearing as a witness then he or she may be cross-examined and opinions then expressed may appear to compromise their independence in future appeals.  I have never known the power to be used other than to obtain a written report from a financially qualified member in child support cases.

51.	However, the change in the tribunals’ powers has made no difference to the appellant’s case, because it is undisputed that the second tribunal could, if it wished, have obtained a medical report.  It had a discretion.  The issue is whether it failed to act judicially in the present case by not adjourning for one.  With some reluctance, I conclude that it did, so that its decision must be set aside.  It was obvious from the appeal papers sent well in advance that they contained no copy of any expert report.  One might have expected a request for postponement at that stage, coupled with a wish to obtain an expert report.  Nevertheless, given the lack of detail in the Commissioner’s recommendation, I appreciate that the appellant and Mr Moore may have been lulled into a sense of false security.  The previous submission from the Secretary of State, which had not been refuted by the Commissioner, suggested that a further report might be helpful.  In those circumstances the tribunal ought to have adjourned, either to allow the appellant to obtain it himself or for the tribunal to direct its provision.

Other grounds of appeal 

52.	I agree with Mr Brown that none of these amount to error in law.  The second tribunal’s findings were extremely comprehensive.  Its clear statement that the relevant accident did not cause the appellant’s acromegaly either by causing a pituitary tumour de novo or by causing mutation of a pre-existing inactive adenoma, plainly show that it adequately considered aggravation.  A psychological condition as a separate result from the relevant accident, divorced from acromegaly, was never raised and so the tribunal was not required to address it.  A tribunal does not err in failing to identify what triggered the appellant’s condition; its jurisdiction is to decide whether the claimant succeeds because he has made out the appropriate qualifying criteria under the legislation.

Proof of a causal link

53.	I have already said that the claimant is an extremely genuine man who passionately believes that the relevant accident caused his acromegaly.  However, on very careful review of all the evidence in the case, the inevitable conclusion is that no reasonable tribunal could infer a causal link having applied the standard of a balance of probabilities.  One does not have to be medically qualified to make this assessment.  Every day, up and down the country, judges evaluate medical and other expert information.

54.	As noted, Dr Reed began her paper by explaining the anatomy, physiology and pathological processes relevant to the case.  No information lodged on behalf of the appellant gives such an explanation and it has not been disputed on the appellant’s behalf.  It is cogent and straightforward and I accept it.  It reads:-

“3.	3.1	There are two types of glands in the body. 

Exocrine glands – These are glands which deliver their secretions via a duct to the part where they function.  For example – the salivary glands (of which there are several), produce saliva which travels to the mouth via ducts; sweat glands which produce sweat which is delivered to the surface of the skin via ducts.

Endocrine – These glands produce secretions which they deliver into the blood stream.  The secretions (known as hormones) travel via the blood to the target organ.  For example – the pancreas produces the hormone insulin which travels in the blood to the liver where it is involved in the metabolism of sugars.  The Pituitary gland is an endocrine gland, which produces several hormones, some of which control other endocrine glands, eg the thyroid gland, the ovaries, to name but two.

3.2	When an endocrine gland produces too little hormone the condition is prefixed with the term ‘hypo’ eg hypothyroidism. When endocrine gland produces too much hormone it is prefixed with ‘hyper’, eg hyperthyroidism.  In all cases of under or over production there is more than one cause.

4.	The Pituitary Gland (also known as the Hypophysis)

	4.1	The Pituitary gland is a reddish-brown, ovoid body measuring 12mm by 8mm.  It is divided into two distinct parts which have separate functions–

		The posterior pituitary (also known as the neurohypophysis)
		The anterior pituitary

	4.2	The posterior pituitary is linked to hypothalamus (a part of the forebrain).  The thin link between hypothalamus and the pituitary gland is referred to as the pituitary stalk.  The blood supply to the whole of the pituitary runs alongside this stalk.  There is no direct connection between the hypothalamus and the anterior pituitary.

	4.3	The pituitary gland is situated in a bony “fossa”, i.e. a cup-shaped, protrusion into the bone of the base of the skull.  The fossa is roofed by a fold of dura mater, through which the stalk passes.  The dura mater is the strong protective skin which protects the central nervous system.

	4.4	The pituitary fossa is deep within the head.  Above it is the rest of the base of the skull, and thence the brain and cranium.  Below it are the bones of the base of the skull; below which are the nasal cavities.  To the sides are bones of the base of the skull which then join to the bones of the side of the skull.  To the front are the bones of the base of the skull; in front of which is the optic chiasma (the point where the optic nerves from the eyes converge together).  Thus the pituitary is very well protected, the most vulnerable part being the pituitary stalk.  However even this part requires considerable force to damage it, and is only associated with very severe head injuries, and is unlikely to occur in a trauma which did not require hospital treatment and an absence from work.

	4.5	Functions of the Pituitary Gland.

The two parts of the pituitary gland have distinct, separate functions (and effectively are two separate glands):

The Posterior Pituitary

The Posterior Pituitary produces a hormone which acts on the kidney to produce concentrated urine.  Without this hormonal control the kidney produce copious amounts of dilute urine, causing the patient to drink excessively.  This under-functioning of the posterior pituitary causes the condition Diabetes insipidus.  (Note this is an entirely different condition to diabetes mellitus – the condition lay people refer to as “diabetes”).  Diabetes insipidus can be caused by several things.  Trauma to the pituitary stalk is one of these causes.

The Anterior Pituitary Gland.

The anterior pituitary gland produces several hormones which target different endocrine glands and organs of the body. E.g. Thyroid stimulating hormones (TSH) stimulates the thyroid gland to produce hormones; Luteinising hormone (LH) and follicle stimulating hormone (FSH) act on the ovaries and the testicles (to name but three examples, there are more, including Growth Hormone).  Different cells produce different hormones.  Growth hormone (GH), as its name implies, affects the growth, and is more produced in childhood and adolescence than in adult life.  However GH is produced throughout life.

	4.6	Hypopituitarism

This term is usually used to describe an under-functioning of the anterior pituitary gland.  There are many causes of this.  Severe trauma to the head is a recognised cause due to the interruption of the blood supply when the blood vessels are damaged as they travel alongside the pituitary stalk.

Hypopituitarism causes a decrease in hormone production NOT an increase.  It is life-threatening condition requiring hormone substitution therapy.

	4.7	Hyperpituitarism

Again the term is usually applied to the anterior pituitary.  As different cells in the anterior pituitary gland produce different hormones, the presentation depends on which type of cell is over-producing.  In the case of Acromegaly it is the cells which produce Growth hormone which are producing too much.  An over production of Growth Hormone prior to the end of puberty causes Gigantism, whereas over production beginning after puberty results in Acromegaly.

4.8	Acromegaly

More than 95% of Acromegaly cases are due to a benign tumour of the pituitary gland, known as a Pituitary Adenoma, ie there is an overgrowth of the cells which produce GH.  Most pituitary adenomas arise spontaneously, though a minority are due to genetic predisposition.

The remainder of cases (5%) are due to ectopic production (i.e. produced outside of the pituitary).  The sites of ectopic production of GH are in the pancreas, kidneys, adrenals and lungs.”

55.	The appellant told me at the hearing that a tumour may cause diabetes insipidus and also hypopituitarism.  There is however nothing in any of the papers he has lodged which support this.  That a tumour plays a part in acromegaly can lead to no inferences, without further evidence, that it may result in diabetes insipidus or hypopituitarism.  Even were it so, that sheds no helpful light on the very different phenomenon of an adenoma due to an overgrowth of cells.  The appellant also relied today, as in his “patient’s story”, on the following point:-

	“Likewise, as with the pituitary adenoma, a blow to a woman’s breast is strongly linked to the development of breast cancer.”

I am aware people have perceptions to this effect but so far as I know, and certainly the appellant has lodged no such evidence, there is no reliable medical support for this theory.

56.	Most of the medical studies supplied by the appellant relate to hypopituitarism.  As Mr Brown said today, this is the very opposite of the appellant’s problem.  Therefore these papers are not relevant to the appellant’s own situation.

57.	Some of the papers lodged indicate that diabetes insipidus can occur following head trauma.  It is medically acknowledged that damage to the pituitary stalk is one of the causes of diabetes insipidus but the appellant does not have this condition.  He was not absent from work after the relevant accident until 1 September 1976 which does not suggest the kind of head injury implicated either in diabetes insipidus or in hypopituitarism.

58.	Some of the information refers to brain tumours.  However, a pituitary tumour is not a brain tumour because the gland does not lie within the brain.

59.	There is a further group of papers which describe the signs and symptoms of acromegaly.  They contain nothing to suggest that acromegaly can result from trauma.

60.	The appellant relies heavily, both at my oral hearing and in the case papers, on what he calls “the Baxter case”.  Baxter is actually the name of the author of a medical article lodged by the appellant, who works as a nurse anaesthetist.  Her article describes the unique problems presented for the anaesthetist when an anterior pituitary tumour is surgically removed.  She begins her paper stating:-

	“This is a case report of a patient who sustained a traumatic head injury, developed symptoms of acromegaly, and subsequently underwent an elective transsphenoidal hypophysectomy for removal of a pituitary adenoma.”

The author is merely confirming the history given by the patient.  The report does not purport in any way to support a proved medical link between a traumatic head injury and the development of acromegaly.

61.	The appellant’s own “patient’s story” and a document called “Steve’s story” are accounts by laymen of the way in which their symptoms developed.  Each one pinpoints a head injury as part of their history.  However, neither provides scientific or medical validation identifying a cause.

62.	Other information lodged covers a variety of points; for example, a paper reporting that there is no evidence that a single incident of trauma can cause cancer, and another paper dealing with life threatening head injuries which suggests that the levels of some of the pituitary hormones remain normal in those who survive such severe injuries but are increased in those who died as a result.  None of this miscellany is helpful to the appellant’s case.  In fact, studies suggesting that there is no evidence that a single incident of trauma can cause cancer does not support the appellant’s own anecdotal view that a blow is strongly linked to the development of breast cancer.  Certainly nothing produced demonstrates any analogy between the mechanisms by which different forms of cancer occur and the processes which result in acromegaly.

63.	There is one paper dated 1972 and with only the title “A case of post-traumatic acromegaly”, which presumably suggests a link between acromegaly and trauma.  The appellant was unable to access the paper (and nor was Dr Reed) so no content is provided.  However, as I mentioned to the appellant at the hearing and it was not meant facetiously:-

			“One swallow does not make a summer”.

This one paper is not enough to establish a causal link between head injury and acromegaly.

Expert evidence submitted since the hearing of the second tribunal

64.	I turn now to Dr Howard’s letter, the crux of which is set out at my paragraph 27.  A neurologist is not a surgeon so Mr Moore is, with respect, incorrect when he states that:-

	“When a Pituitary Tumour is diagnosed a Neurologist will remove the tumour…..  
	Neurologists… are concerned with the make up and causes of the tumour”.

65.	Prior to lodging the consultant neurologist’s report, Mr Moore argued that the expert witness should be an oncologist.  An oncologist is one who makes a study and treatment of tumours.  Mr Moore then regarded this as preferable to using an endocrinologist, i.e. a doctor who studies the structure and physiology of the endocrine glands.

66.	A neurologist’s expertise is in the nervous system.  I have already set out Dr Reed’s qualifications.  On the face of it neither doctor, and I take into account Dr Howard’s consultant status, seems more experienced than the other about acromegaly.  Dr Howard does not claim that it is his particular area of expertise.

67.	Dr Howard’s first quoted paragraph confirms the undisputed diagnosis of acromegaly.  He then links the psychiatric disturbances as possibly related to the acromegaly.  This of course has no bearing on any causal link between that acromegaly and the relevant accident.

68.	It is only in his last paragraph that Dr Howard deals with the causal link.  His first two sentences concern damage to the pituitary stalk and he immediately acknowledges that the relationship of head trauma to acromegaly “is a little less certain….”.  There is nothing here which could support a link on a balance of probabilities between this appellant’s acromegaly and the punch to his head.

69.	He then continues:-

	“….but there are a number of very clear reports indicating a temporal association between a head injury and the development of acromegaly.”

70.	However, he provides no references in the literature for such reports.  In order to accord weight to such evidence, various factors are material.  One needs to know the relevant qualifications and experience of the authors.  If the reports’ conclusions are based on primary research, then an adjudicative body must take account of the date of such research, its purpose and methodology and the details of its findings.  In so far as Dr Howard draws his conclusions from a survey of medical papers, not only the appropriate references are required but the process of selection of the relevant literature.

71.	In any event, even standing such reports, that a temporal association has been noted between a head injury and the development of acromegaly does not yet establish as fact on a balance of probabilities that the one is caused by the other.  The law regards it as illogical to ascribe the cause of a result to an event simply because the one followed the other.  It may be that indications of a temporal association between two kinds of event become so overwhelming as to suggest a causal relationship.  But no such evidence has been adduced in this case.  Certainly, one cannot draw such an inference without evaluating the precise data and conclusions of the reports mentioned.    

72.	In contrast to Dr Howard, Dr Reed states:-

	“A thorough search of both text books and the internet has failed to link hyperpituitarism, and in particular acromegaly, with head trauma, either as a direct cause of it or as having an exacerbating effect”.

As the appellant has avowedly trawled the internet and the evidence produced does not support his proposition and because there is no reason to doubt Dr Reed’s statement, I accept it.

73.	That the appellant and other patients with pituitary dysfunction have been asked by doctors, “Have you ever suffered a head injury?”, (as put to me in evidence by the appellant at the hearing), does not prove a causal link between head injury and acromegaly.  Quite apart from the fact that such patients include those who suffer from other conditions than acromegaly, their answers are relevant to ongoing research (which I do not doubt exists) into the very puzzle which the appellant would like to have solved i.e. what causes the excess of cells which produce growth hormone.  But crucially no evidence has been produced of research which already substantiates that, on a balance of probabilities, an accident such as the relevant accident has any causal link with, or has an exacerbating effect on, the development of acromegaly.

Summary

74.	Accordingly, I substitute a decision in the terms set out above at paragraph 1.

						(Signed)
						L T PARKER
						Commissioner
						Date:  11 December 2003