MTBI typically induces a range of symptoms such as: headaches, blurred vision, poor concentration, sleep disturbance, depressed mood or irritability. These post-injury effects are referred to as Post-Concussion Syndrome (PCS), a transient condition which is thought to reflect a fully recoverable disturbance of neural function [2-5]. However, long beyond the typical recovery interval of one to three months, at least 15% of persons with a history of MTBI continue to see their GPs because of persistent problems [6-10]. The clinical validity of these sequeale is not undisputed, in part because there is no readily evident physiological damage or deficit that could be made accountable. Consequently, a range of alternative explanations such as involvement in litigation [1] and pre - morbid psychological problems [11] are discussed. In addition, one may question the correctness of the assumption that MTBI is fully recoverable in all cases.

The view that MTBI leads to transient disturbances only is further supported by the absence of structural brain damage in diagnostic MRI images acquired with standard recording sequences[12]. However, the combination of high resolution MRI with specifically tailored scanning protocols provides evidence for microstructural abnormalities in MTBI patients [13-15]. Ultra-structural studies further indicate that MTBI may damage the structure of neurofilaments and cause traumatic axonal injury [16,17]. Together, these findings support the idea that MTBI can introduce primary structural damage in reaction to the axon misalignment, disconnection and swelling that occurs in response to the physical forces inflicted on the neural tissue [17-19]. It therefore appears plausible to assume that microstructural damage can persist, and that this tissue damage may form the pathophysiological foundation of the persisting sequeale some MTBI patients' experience. This assumption gives rise to the hypotheses that the neural damage affects information processing, and henceforth the prediction that only those MTBI patients who suffer chronic PCS symptoms show neurobehavioral deficits.

This idea is not new and various research groups have studied the role of neurobehavioral performance in PCS. However, the existing data do not provide a coherent picture as to whether cognitive performance in longterm MTBI patients is disturbed or not, and if, to what extent symptoms and performance are related. While some studies report a lack of evidence for sustained postconcussive effects of MTBI [20,21], others report general cognitive deficits [22-24], as well as impairments in specific information processing domains such as attention [25,27], working memory [26,27], and processing speed [28]. Two meta-analyses highlight this empirical controversy and come to the conclusion that the relationship between PCS and cognitive impairment is 'generally weak' [29,30].

We propose that the inconsistent findings on the relationship of neurobehavioural performance and PCS might, in part, be due to the fact that most experiments investigated long-term MTBI consequences by studying a cohort of MTBI participants without taking the status of PCS specifically into account. However, it is clear that only a subgroup of MTBI patients continue to report PCS symptoms, and hence a separate assessment of MTBI patients with and without sustained PCS should provide a further insight. The incoherent picture emerging from the literature represents a serious problem for both suffers and health care providers. For example, little diagnostic advice is provided for clinicians regarding the classification and prognosis of PCS, and ICD-10 suggests guidelines for research purposes only. Furthermore, the chronic effects of MTBI compromise quality of life and general well being [30], and given the high incident rate of MTBI, particularly amongst young adults, the socio-economic consequences are drastic [2]. Henceforth there is a need to characterise and understand chronic MTBI effects. In this context, the present experiment studied cognitive performance in a cohort of MTBI patients at least 12 month post-incident, whereby those with and without PCS were studied separately. To control for potential confounding factors, all participants were in employment or studying at University and were not involved in any litigation.

Our study further revealed interesting results on the role of loss of consciousness in sustained PCS and/or its severity. According to ICD - 10, a 'history of head trauma with loss of consciousness preceding the onset of symptoms by a period of up to four weeks' represents one of the diagnostic criteria (criterion 'B'). However, in our experiment 4 out of 11 participants in the PCS⁺ group (36%) had not experienced loss of consciousness but nevertheless satisfied all other PCS criteria. At the same time, 14 out of 27 participants (52 %) in the PCS^- group had lost consciousness during the incident but did not develop chronic PCS. This is consistent with other studies [41,42], where PCS was found in the absence of loss of consciousness. Most notably in this context, Umile et al. [15] recently reported that participants with PCS performed poorer in neuropsychological tests and showed structural abnormalities in high-resolution MR scans after MTBI without loss of consciousness. Together, these and our findings provide initial evidence that a critical re-evaluation of the loss of consciousness criterion in ICD-10 may be considered. Of course one may argue that our findings on loss of consciousness are of questionable reliability, due to the circumstances under which the majority of incidents occur. However, the patient themselves typically remain the only source of information, henceforth the subjectively perceived loss of consciousness - whether it was truly experienced or not - is probably of limited diagnostic value.

A further aim of the present study was concerned with characterizing potential neurobehavioral correlates of sustained PCS. Based on the hypothesis that mild brain injuries may involve minimal structural damage, we presumed that sustained PCS should be reflected in diminished performance during cognitive tasks. To this end, a correlational analysis of test performance and symptom severity, indexed by the RPQ scores, revealed positive correlations with error rates for 50% of the neurobehavioral subtests in the PCS⁺ group. Thus, our data clearly suggests that PCS severity is associated with objectively measurable performance deficits in some cognitive tasks. These results highlight the fact that only those MTBI participants who suffer from PCS show deficits in cognitive processing, and provide further evidence that the level of PCS severity and not the experience of MTBI per se is the critical factor. The findings obtained by the correlational analysis have further importance with regards to the often criticized 'unspecific everyday' nature of the RPQ symptom checklist. Studies have shown non-clinical groups to report symptoms similar to those with PCS (e.g. [39]), which led to claims that the RPQ is an unreliable measure for PCS diagnosis (e.g. [43,44]). However, the absence of a systematic relationship between RPQ and cognitive performance indices in the PCS^-/control groups, but highly correlated scores in the PCS⁺group found in the present study, identify the RPQ as a valid diagnostic measure despite the unspecific nature of checklist items [4].

The assessment of neurocognitive function revealed significantly poorer response accuracy in the PCS⁺ group than in PCS^- and controls, but no systematic effects for reaction time. This leaves three possible explanations. One could either conclude that persisting PCS is unlikely to affect a person's speed of response to stimuli, that RT non-result is due to low test power and thus an effect of sample size, or that participants in the PCS⁺ group may have greater motivation to perform well in the task. The latter explanation is strongly supported by Potter et al. [24], who suggested that some people with MTBI have heightened anxiety in novel testing situations, because of fears that their performance is affected by their condition. As a result, these participants may be in a state of higher arousal which impacts on their response execution time. For the present study, Potter's argument gains further credibility when error rates are taken into the equation. Thus, participants in the PCS⁺ group showed higher error rates than participants in both other groups, while reaction times were unaffected. Peloso [44] further argues that the simultaneous management of response accuracy and response speed becomes less efficient when the cognitive load exceeds a certain threshold level, and that this level may be lower following minor brain damage. This idea is well compatible with our finding that the highest error rates were found for the subtests with greatest cognitive demand. Furthermore, cognitive and emotional problems are known to persists longer after the incident than somatic symptoms [45]. In line with this observation, the RPQ symptom profile shows that the experienced symptoms in the PCS⁺ group relate mostly to cognitive processing, with poor concentration and irritability receiving the highest scores.

A continuing controversy in the discussion of chronic PCS concerns other contributing factors such as malingering [11,46-49]. These concerns are partly driven by the lack of clear evidence for objectively measurable correlates of PCS. We cannot totally rule out the possibility of malingering or other contributing factors to our findings. However, this influence is probably of negligable magnitude for several reasons. First and foremost, participants involved in litigation of any kind were excluded from the study. Secondly, our volunteers were in employment or studying, and generally in good health and spirits. Finally, the severity of PCS symptoms systematically varied with the level of performance across a range cognitive tasks, and such a data distribution across a group is unlikely to be explained by malingering or exaggerated responses in the RPQ.

The research hypotheses of the present paper were based on the assumption that mild head injury can cause permanent microstructural damage and disturbances of neural function. As a result, information processing may become less efficient or more effortful and lead to deficits in neurobehavioral performance. Of course the question regarding the neural origin and mechanisms underlying sustained PCS are not addressed in the present study, however the data is in line with these ideas. Only a subgroup of MTBI participants show PCS symptoms, cognitive failures in everyday situations and diminished neurobehavioural performance in standardized test batteries. This neuroscience-based interpretation of our data might be challenged by the view that sustained PCS is driven by psychological factors rather than structural consequences of brain damage [45,53,54]. For example, Van Zomeren [55] and Wong [56] argued that PCS related symptoms may be manifested to compensate for 'behavioural faults' which patients attribute to the head injury. While this theory could explain why common complaints reported in the PCS⁺ group are more psychological in origin than somatic, it falls short of a plausible explanation for the strong correlation of objectively measurable performance indices and symptom severity.