RESEARCH LETTERS Oxford Brookes University, London Road, Headington, Oxford OX3 7PD UK (A J Lloyd); and Faculty of Medicine, University of Leicester, Robert Kilpatrick Building, Leicester Royal Infirmary, P O Box 65, Leicester LE2 7LX, UK THE LANCET • Vol 353 • February 20, 1999 645 Patients’ ability to recall risk associated with treatment options A J Lloyd, P D Hayes, N J M London, P R F Bell, A R Naylor Many practitioners have expressed concern about patients’ ability to understand and recall information about the risk associated with treatment options. A search of medical articles however has revealed very little systematic research in this area. 1 We report a systematic study that analysed patients’ recall of the risks related to carotid endarterectomy (CEA). CEA is a prophylactic surgical procedure that is done to reduce the chance of embolic stroke. 2 The risks associated with surgery and best medical treatment are well understood for this patient group. 3 The operation will reduce but not abolish the risk of stroke, and in a small proportion of patients it will cause a stroke. The operation has an associated stroke risk of 5–7%. 2,3 Patients who are suitable for surgery were all counselled in the clinic by a consultant in the same manner. Patients were informed that their chance of suffering a stroke in the next three years if they didn’t have the operation was approximately 22%. 2 The risk of suffering a perioperative stroke as a result of CEA was also highlighted. At our own hospital this risk is 2·3%, which was determined from an audit of our last 450 CEAs. 71 patients on the waiting list for CEA were sent a quetionnaire 1 month after their clinic appointment (56 responded). This questionnaire was designed to assess patients’ understanding of the risks associated with the different treatment alternatives. Patients were asked to recall their risk of suffering a stroke with each of the treatment options. Patients consistently failed to recall their risk of stroke. Most patients remembered if they proceeded with surgery then their longterm risk of stroke would be reduced. However, over 10% of patients thought that their risk of suffering a stroke at the time of CEA was at least 50%. More worrying was the finding that some patients thought that there was no risk of stroke associated CEA and 11% of patients simply did not know. Only one patient was able to quote the risks that he was told. Patients’ responses are summarised in the table. This study suggests that either patients have very little understanding of the risks and benefits associated with a prophylactic procedure (CEA) or they quickly forget them. One of the main findings of the recent enquiry by the General Medical Council into the conduct of the Bristol heart surgeons was that parents were misinformed about the risk associated with surgery. In the Bristol scenario many months or years after the consultation, parents testified that they were unable to recall accurately the risks associated with paediatric cardiac surgery. Although the present study examines a different operation and patient cohort, it seems fairly clear that patients’ recall of statistical data related to risk is limited, even in the short term. Our survey suggests that informed consent based on verbal information alone is not enough, and that an information letter should be given to each patient as a part of the process of informed consent. 1 Redelmeier DA, Rozin P, Kahneman D. Understanding patients’ decisions: cognitive and emotional perspectives. JAMA 1993; 270: 72–76. 2 European Carotid Surgery Trialists’ Collaborative Group. MRC European Carotid Surgery Trial: interim results for symptomatic patients with severe (70%–99%) or with mild (0%–29%) carotid stenosis. Lancet 1991; 337: 1235–43. 3 North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade stenosis. N Engl J Med 1991; 325: 445–53. Patients’ responses, Actual risk range (mean) Risk of stroke without operation 22–100% (57%) 22% Risk due to CEA 0–65% (10%) 2% Patients’ recall of the risk of stroke without the operation and as a result of CEA Analysis of the monoamine oxidase genes and the Norrie disease gene locus in narcolepsy Helga Koch, Ian Craig, Meryl Dahlitz, Richard Denney, David Parkes Narcolepsy is linked to both HLA class II and non-HLA genes. Most cases are of unknown cause, but abnormal REM sleep symptoms suggestive of narcolepsy have been described in association with Norrie disease. 1 This is an X- linked recessive disorder causing ocular atrophy. Monoamine oxidase (MAO) genetic and biochemical defects occur in some of these subjects and the gene for Norrie disease is in close proximity (within 100 kb) to both MAO A and B coding sequences. 2 We report on the Norrie disease gene area in narcolepsy. We studied markers embracing the Norrie disease chromosomal area in Xp11.3/p11.4 (tel- MAOA-MAOB-ND-cen) in 28 subjects with definite narcolepsy, all with cataplexy (16 male, 12 female, 27 white, 1 black, 20 HLA DR2 positive, 8 DR2 negative) and 49 (DR2 positive control patients with normal sleep-wake habits (33 male, 16 female, all white). No patient had Norrie disease. We looked for microdeletions in the Norrie disease coding region by polymerase chain reactions using primer sets for exons one, two, and three. 3 We also genotyped for a series of microsatellite markers covering the 5' regions of MAOA and MAOB genes. These should identify both intragenic and promoter-region mutations. For MAOA these were the dinucleotide repeat markers from intron 2 and a variable number tandem repeat (VNTR) marker from intron 1; for MAOB, a dinucleotide repeat in intron 2, and novel repeats in introns 1 and 3, a novel VNTR in intron 3, and a novel dinucleotide repeat 22 kb 5' to the first exon. No rearrangements or microdeletions of the Norrie disease gene were detected in any individual. Allele patterns across the MAO gene markers are shown in the table. Both MAOA and MAOB gene markers showed differences between narcoleptics and controls (MAOA: VNTR in intron 1, by clump analysis, p=0·05; MAOB: (CA) n dinucleotide repeat marker in intron 2, p=0·07). The MAOB 181 bp allele was twice as common in narcoleptics as controls. No major variation in allele pattern was detected between the 20 HLA DR2 positive and 8 DR2 negative narcoleptics. The loci examined are X-linked, with straightforward haplotype analysis in males. Both narcoleptics and controls shared haplotype patterns but there were no complete haplotypes in common between the two groups. Comparisons were made between haplotypes centred on the MAOA VNTR and the (CA) n dinucleotide repeat in intron 2 of MAOB. 4 of 5 haplotypes in DR2 positive narcoleptics containing the 340 bp MAOA VNTR were in association with 181 bp alleles at the MAOB (intron 2(AC)n) marker compared with 5 of 12, respectively, in cDR2 postive controls. Furthermore the controls showed a high frequency of a partial haplotype centred on the 340 bp MAOA allele that was not observed in