The paper by Meares and colleagues1 in this issue of J Neurol Neurosurg Psychiatry concerns the implications of defining a syndrome by symptoms that have a high base rate of occurrence in the general population or in other syndromes (see page 300). The issue of neglect of base rates was raised five decades ago in the seminal work of Paul Meehl,2 who pointed out that “the chief reason for our ignorance of the base rates is nothing more subtle than our failure to compute them” (page 234). There are now systematic collections of base rate data in the general population3 and in groups relevant to neuropsychology,4 and websites where national statistics are posted (www.statistics.gov.uk).

Symptoms of postconcussion syndrome (PCS) are rife in the general population (www.statistics.gov.uk) (eg, 29% complain of sleep problems, 27% of fatigue and 20% of irritability, figures that are stable across ages 16–74 years). There are figures for other symptoms of PCS. In various studies, 26.2% of students reported irritability and 16.5% had concentration problems (see page 6 in McCaffrey and colleagues3); 41.6% of 18 year olds reported impulsivity and 33.3% reported inattention (see page 45 in McCaffrey and colleagues3); in women aged 45–54 years, 60% reported memory problems over the past 6 months, 60% reported headaches and 72% reported irritability (see page 58 in McCaffrey and colleagues3); 26.5.% of 17–26 year olds reported word finding lapses (see page 109 in McCaffrey and colleagues3).

There are implications of defining a syndrome with high base rate symptoms. Firstly, the diagnosis will often be plain wrong (eg, a horse is a large animal with four legs but one would not “diagnose” a giraffe or a rhinoceros as a horse). Secondly, the supposed cause of the syndrome is likely to prove not the cause at all (eg, brain injury cannot be the cause of PCS as the same symptom cluster is found in non-brain conditions). Thirdly, diagnosis will not identify an aetiology (eg, as PCS is not specific to traumatic brain injury, the presence of PCS is not “diagnostic” of having had a brain injury). Once recognised that the presumed aetiology of a syndrome is not correct, the syndrome has to be revised or withdrawn from use, otherwise there will be a mis-formulation of the clinical picture and the potential for mis-treatment (ie, the wrong treatment arising from wrong assumptions).

Finally, Meares’ paper is a reminder to be alert to the hidden effects of base rates. For example, gaps in memory are commonplace (memory is not literally continuous, there is normal forgetting, sometimes nothing new happens to remember, we may not notice some aspects of events which others do). Therefore, it is all too easy to examine retrospectively the events surrounding an accident and find gaps in memory that can lead to the erroneous diagnosis of post-traumatic amnesia or to its overestimation. A second example is the diagnosis of dysexecutive syndrome. There is a base rate of executive inefficiency: we all find it easier to concentrate on one thing at a time, all have cognitive lapses, and are all more emotionally labile and irritable at times of stress. Therefore, it is again all too easy to look at a post accident picture and elicit descriptions of dysexecutive syndrome.