Articles & Updates

By Carol Jackson, Solicitor at Pannone and Mike Barnes, Professor of Neurorehabilitation

This article provides an overview of the functions of the pituitary gland, how it can be damaged in an accident and present symptoms in conjunction with a brain injury. We highlight some of the legal and medical issues which arise, and guidance within the context of brain injury claim when the pituitary function should be tested.  Whilst it has been known for many years that pituitary dysfunction can follow traumatic brain injury, it is only recently coming to the attention of medico legal experts and lawyers working in the field of TBI. The relationship between TBI and pituitary dysfunction is now being reported in quality medical peer review journals (see reference list below).

This article outlines to practitioners what they can do as lawyers to help clients with this condition. Whilst there is no totally accepted figure, most studies have found around one third of people after traumatic brain injury have at least temporary dysfunction of the pituitary gland. In many people this dysfunction lasts beyond the acute phase and will be a serious, but treatable, cause of unnecessary further disability. As lawyers, we have long since moved away from the position where personal injury was just about damages; rehabilitation and quality of life are all important. One of the significant features of this condition is that it is treatable, presenting us with the opportunity to improve the quality of life for those with TBI.

Background to Pituitary Function
The pituitary gland lies at the base of the brain and is connected to the brain by a small stalk with direct neural links to the hypothalamus.  It is a vulnerable structure that can be easily damaged in brain injury. The gland is divided into two parts - the anterior lobe and the posterior lobe. The anterior lobe is responsible for the production of growth hormone (GH), luteinising hormone (LH), follicle stimulating hormone (FSH), adrenocorticotropic hormone (ACTH), thyroid stimulating hormone (TSH) and prolactin. In turn the regulation of these hormones is largely under the control of the hypothalamus.  The posterior pituitary gland produces arginine vasopressin (AVP) which has a key role in maintaining fluid balance in the body. It also produces oxytocin which stimulates uterine contraction during birth and ejection of milk during lactation.

Anterior pituitary dysfunction
Growth hormone deficiency causes growth failure or slowing of growth in children.  In adults growth hormone deficiency can cause decreased energy, an increase in fat and decrease in muscle mass. There should be a high index of suspicion if a child is beginning to show slowed growth after a traumatic brain injury. In adults growth hormone deficiency can be easily overlooked as the symptoms of decreased energy and tiredness and increased weight are very common in any case after brain injury.

FSH-LH - The production of these hormones can cause problems with the menstrual cycle, loss of libido, hot flushes, dyspareunia (pain during sexual intercourse) and infertility in women. In men it is often associated with loss of libido, impaired sexual functioning as well as mood impairment, loss of facial, scrotal or trunk hair and decrease in muscle bulk and easy fatigue. Once again these are problems that are quite common after brain injury and diagnosis is not always obvious.

ACTH - Chronic ACTH deficiency is also associated with fatigue, anorexia, weight loss and sometimes other metabolic complications such as low sodium and sugar levels. In children it can present with delayed puberty and failure to thrive. In more severe cases ACTH deficiency can be associated with vascular collapse, particularly during superimposed illness.

TSH - TSH is the hormone that stimulates the thyroid gland to produce thyroxine. Individuals with TSH deficiency manifest the symptoms of hypothyroidism. These symptoms can include tiredness, coldness, constipation, hair loss, dry skin, hoarseness, general lethargy, including slowing of "cognition”, weight gain and low blood pressure.

Prolactin - Fortunately there is no clinical syndrome that is known to be associated with prolactin deficiency.

Testing / Treatment of anterior pituitary function
Clinically the treatment is to refer patients to a local endocrine department if there are concerns about the pituitary function. This is not as easy as appears given that many of the symptoms are very similar to those arising from TBI, especially tiredness, lethargy, mood impairment and loss of libido.

From the medico legal perspective the starting point is to review the A & E and medical records and send the notes to the expert neurologist to obtain an opinion on whether any of the client’s symptoms could be caused by problems with the pituitary function. There are factors which mean some cases merit closer attention and may prompt the lawyer to investigate and refer:

• those cases which involve a  more severe head injury
• basal skull fracture
• a client with diabetes insipidus in the acute phase

These conditions should have been recorded in the A& E notes and are factors which raise the chances that there has been damage to the Pituitary gland. It is of key importance that the medico legal neurologist reviews the notes to give a clinical view which supports further investigations. If the neurologist opinion is positive and confirms the suspicion of damage to the Pituitary gland it is most important the client is referred to a specialist endocrinologist who is fully conversant with this condition. A general endocrinologist will not suffice; it will be essential to check out the specialist  via his CV, or direct questioning.

Simple blood tests of the hormones are not usually adequate as the pituitary gland needs to be "dynamically" tested. Provocative tests stimulate hormone release either indirectly (by, for example, injecting a small dose of insulin) or directly by injecting synthetically manufactured peptides (Synacthen). Other tests are possible such as a glucagon stimulation test or an oral glucose tolerance test. This is clearly a specialist area and it is important to emphasise that simply taking blood to measure the hormones is not adequate.

Posterior Pituitary function
AVP deficiency leads to cranial diabetes insipidus which is not to be confused with a "sugar" diabetes mellitus.  This condition causes the passage of large volumes of dilute urine (often more than three litres per day). This can obviously lead to dehydration and severe thirst. It is a disorder well recognised and quite common in the acute phase of traumatic brain injury but can extend for many months or years after the injury. Diagnosis is usually quite straightforward by measuring urine osmolality before and after administration of the AVP analogue called desmopressin. However endocrine referral is generally needed for diagnosis and long term follow up. The treatment is usually straightforward and is by administration of desmopressin (DDAVP). 

There is no known role for oxytocin production in men but in woman oxytocin is probably necessary for the regulation of lactation and birth and reproductive behaviour but relatively little seems to be known about the effect of lack of production.

Screening and Treatment
A key factor is the ability to treat and relieve the condition. For many clients, excessive fatigue is often one of the most debilitating aspects of a brain injury and can be a barrier to work and social integration. Lack of sexual drive may aggravate relationship problems which commonly occur after a brain injury.

Treatment for all the Pituitary  related conditions  is simply by the administration of the appropriate hormones and thus it is important to identify this condition as some, if not all, of the unpleasant symptoms can be readily alleviated.

The costs of the investigation based upon the recommendation of the neurologist would be recoverable in the case. The ongoing treatment recoverable either on NHS or privately for life on the appropriate multiplier and potentially could have significant impact on the value of the case. The benefits to the client  are  intangible.

Should we undertake screening? Ideally everyone after a traumatic brain injury should have pituitary function screening but this is unlikely to happen and indeed has serious resource implications for the NHS.  The problem is that many of the symptoms of pituitary dysfunction overlap with symptoms that are common in any case after traumatic brain injury. At the moment there are no clear guidelines. Pituitary dysfunction is commoner after severe brain injury and after basal skull fracture so perhaps those people should be screened. Those who develop diabetes insipidus in the acute phase should also be followed up and screened.  This article simply flags up to treating physicians, medical experts, and personal injury lawyers   that there should be a low threshold for considering pituitary dysfunction. It is an easily treated problem and one that deserves greater recognition.

Further Reading

1. Norwood KW, Deboer MD, Gurka MJ et al.  Traumatic brain injury in children and adolescents: surveillance for pituitary dysfunction. Clin Pediatr 2010; 49: 1044-9.  (This article showed that 16% of children after traumatic brain injury had growth hormone deficit as well as lower levels of thyroxine, follicle stimulating hormone and (in males) testosterone).
2. Guerrero AF, Alfonso A. Traumatic brain injury-related hypopituitarism: a review and recommendations for screening combat veterans.  Mil Med 2010; 175: 574-80.  (This is a general review that show that the prevalence of hypopituitarism rises to 30-80% even after 24-36 months following traumatic brain injury)
3. Gasco V, Prodam F, Pagano L et al. Hypopituitarism following brain injury: when does it occur and how best to test? Pituitary 2010; Jun 5 (Epub ahead of print). (This is a review article of the whole subject and suggests that screening should be carried out after severe brain injury and in particular those who fracture the base of the skull or have diabetes insipidus).
4. Blair JC. Prevalence, natural history and consequences of posttraumatic hypopituitarism: a case for endocrine surveillance. Br J Neurosurg 2010; 24: 10-7.  (A general review article of the subject).
5. Krahulik D, Zapletalova J, Frysak, Vaverka M.  Dysfunction of hypothalamic-hypophysial axis after traumatic brain injury in adults. J Neurosurg 2010; 113: 581-4.  (This is one of the largest studies of hypopituitarism after traumatic brain injury. The author found 19 patients (21%) had primary hormonal dysfunction including significant deficit in growth hormone hypogynerium and diabetes insipidus.  There was a link with severe brain injury and low Glasgow outcome scale scores).
6. Urban RJ, Harris P, Masel B. Anterior hypopituitarism following traumatic brain injury. Brain Inj 2005; 19: 349-58. (This is one of the more thorough articles that reviewed the prevalence of hypopituitarism after traumatic brain injury and found that between one half and one third of people after TBI had antipituitary hormone deficiencies, particularly growth hormone and thyroid deficiencies). 
   

Carol Jackson is a Partner in the Serious Injury team at Pannone

If you need further advice on this subject we will be pleased to hear from you.  Freephone or 0800 0384 384 or view Carol's profile.