The role of pharmacotherapy in the management of behaviour disorders in traumatic brain injury patients.

The aim of this paper was to systematically review the research published in English language on the effectiveness of drugs for the treatment of neurobehavioural disorders in patients with traumatic brain injury (TBI). A literature search using Medline, Pre-Medline, Embase, Psychlit and Cochrane Library databases between 1990 and January 2003 as well as a hand search of Brain Injury since 1996 were carried out. Phrases such as 'head injury', 'brain injury', 'drug treatment', 'drug trials' and 'randomized controlled trials' were used. Sixty-three papers were selected for data synthesis. Of these, 13 were randomized controlled trials, eight were prospective observational studies, four were retrospective studies, 25 were case series and 13 were single case studies. There was a dearth of type I-III evidence. There was no strong evidence either way to suggest that drugs are effective in the treatment of behaviour disorders in patients with TBI. However, there was weak evidence, primarily based on case studies that psychostimulants are effective in the treatment of apathy, inattention and slowness; high dose beta-blockers in the treatment of agitation and aggression; anti-convulsants and anti-depressants (particularly SSRIs) in the treatment of agitation and aggression, particularly in the context of an affective disorder; and possibly a specific neuroleptic methotrimeprazine in the treatment of agitation in the post-acute stage of Acquired Brain Injury. Some drugs that are effective in some patients have been shown to be ineffective in others. Some drugs, particularly lithium and dopaminergic drugs could cause adverse effects and deterioration in some patients.

Is there an association between life events, postnatal depression and thyroid dysfunction in thyroid antibody positive women?

BACKGROUND: Postnatal depression is more common in women positive for thyroid autoantibodies, independent of thyroid hormone dysfunction, but the basis of this association is unclear. AIMS: The objective of the work reported here has been to investigate from data obtained from previously published research, a possible association between life events, postnatal depression and the development of thyroid dysfunction in women who are positive for thyroid autoantibodies. METHOD: A cohort of pregnant women whose thyroid antibody status was positive (N = 115), was identified at antenatal booking (approximately 16 weeks). These, and a group of women negative for thyroid antibodies (N = 123), were assessed for depression at six to eight weeks postpartum and then at 12, 20 and 28 weeks postpartum according to Research Diagnostic Criteria (RDC). The number and type of life events over the preceding year were also assessed at eight weeks postpartum using Paykel's Life Event Schedule. At four weekly intervals post-partum until six months, thyroid antibody levels and thyroid function (plasma T3 T4 and TSH) were measured. RESULTS: As anticipated, the thyroid antibody status remained the same throughout the study, and there was no difference in the number or type of life events reported in the preceding year, between antibody positive and antibody negative women. Postnatal depression was associated with an excess of both total and negative life events, independent of thyroid antibody status or actual thyroid hormonal status. Women who developed thyroid dysfunction did not report an excess of life events (total, negative or neutral) in the preceding year. CONCLUSION: There was an excess of reported total and negative life events in women with postnatal depression, but this was independent of thyroid antibody status or function.