Question 36#

All of the following are necessary to establish the competence to make a will except:

A. The person should know what the act of making a will means

D. Testamentary capacity refers to the competence for drafting and signing a will. In English law, this is based on case Banks v Goodfellow in 1870. The capacity to draw a will requires:

1. Understanding the nature of the act of drawing a will and its effects
2. Understanding the extent of the property being disposed
3. Understanding the nature and extent of the claims of those who are included or excluded in the will
4. Absence of mental disorder that can affect the previous (1–3) competencies
5. Absence of undue influence (duress) by third parties

Hence a mentally ill individual can have full testamentary capacity if his/her mental illness does not directly influence his/her understanding of the process, the extent of his/her estate, or the nature of claims that could be made to his/her estate.

Reference:

1. Murray B and Jacoby R. The interface between old age psychiatry and the law. Advances in Psychiatric Treatment 2002; 8: 271–278.

Question 37#

Compared with mania at younger age of onset, late-onset mania in elderly people is characterized by:

A. Stronger genetic loading

D. Late-life mania is often different from earlier onset mania. There is a prominent mixture of depressive symptoms in late-life mania; in addition, those with late-onset mania are more likely to have had a depressed phase during their fi rst admission. Occasionally, manic symptoms in late life may herald the onset of frontal-type dementia. It is also shown that men may have higher rates of mania in late-life than women – one series reported a difference of 60% in men to 10% in women. A significant association with cerebral organic disease has been demonstrated, leading to the term secondary mania in cases with organic aetiology. A higher tendency to fi nd vascular lesions in neuroimaging studies of older manic patients has been described. Similar to geriatric depression, late-life mania is also said to have less genetic contribution to aetiology than younger adults with mania.

Reference:

1. Murray R, Kendler K, et al., eds. Essential Psychiatry, 4th edn. Cambridge University Press, 2008, p. 369.

Question 38#

Which of the following anti-dementia drugs acts directly on nicotinic receptors to increase cholinergic neurotransmission?

A. Memantine

D. Tacrine, donepezil, and galantamine selectively inhibit acetylcholinesterase. In addition galantamine also improves cholinergic neurotransmission by acting as an allosteric ligand at nicotinic acetylcholine receptors to increase presynaptic acetylcholine release and postsynaptic neurotransmission. Rivastigmine inhibits butyrylcholinesterase in addition to its inhibition of acetylcholinesterase. Butyrylcholinesterase forms around 10% of the total cholinesterase in normal human brains and it is mainly associated with glial cells. With the progression of dementia, it is noted that acetylcholinesterase activity decreases while butyrylcholinesterase activity stabilizes or even increases in relation to glial proliferation. This may lead to changes in the ratio of acetylcholinesterase to butyrylcholinesterase. To date, a significant difference in the clinical efficacy of rivastigmine compared with donepezil or galantamine in advanced dementia has not been demonstrated.

Reference:

1. Scarpini E, Schelterns P, and Feldman H. Treatment of Alzheimer’s disease; current status and new perspectives. Lancet Neurology 2003; 2: 539–547.

Question 39#

The plasma half-life of memantine is approximately:

A. 2–4 hours

C. Memantine is a non-competitive NMDA antagonist that prevents excess calcium from entering the neurons leading to a neuroprotective effect. It is completely absorbed from the gastrointestinal tract with a bioavailability of 100%. Memantine exhibits linear (first order) pharmacokinetics over the entire dosage range of 10–40 mg/day. It rapidly passes the blood–brain barrier within 30 minutes of absorption. Forty-five per cent of the drug binds to plasma proteins. It is metabolized by glucuronidation, hydroxylation, and N-oxidation. Seventy-five to 90% of the drug is eliminated via the urine, with 10–25% of the drug eliminated in the bile and faeces. The elimination half-life is about 60–80 hours. Excessively alkaline urine can decrease the excretion.

Reference:

1. Robinson DM, Keating GM. Memantine: a review of its use in Alzheimer’s disease. Drugs 2006; 66: 1515–1534.

Question 40#

The anticholinesterase agent with least drop-out rates in longitudinal trials is:

A. Galantamine

C. Head-to-head comparisons of anti-dementia drugs show similar effects on measures of cognition and behaviour for rivastigmine, galantamine, and donepezil. But the analysis of withdrawals before the end of the study period showed significant differences between donepezil and other medications in the group – especially rivastigmine. Similarly, a meta-analysis that compared the effect of galantamine, rivastigmine, and donepezil on safety (drop-outs due to adverse events) and selected cognitive outcomes showed a comparable benefit on ADAS-Cog scores compared with placebo for all three drugs; a dose-related effect was observed for donepezil and rivastigmine but not galantamine. There was evidence for increased drop-out rates with both galantamine and rivastigmine compared with donepezil.

Reference:

1. Tyrer P and Silk K., eds. Cambridge Textbook of Effective Treatments in Psychiatry. Cambridge University Press, 2008, p 224.