Studies on head trauma complications with special reference to Mild Traumatic Brain Injury

Sammanfattning: Traumatic brain injury (TBI) is a recognised public health problem. Patients with mild traumatic brain injury (MTBI) represent the main part of the total TBI population attending hospital. The aim of this thesis was to study some clinically important aspects of post-acute complications and long-term consequences after head trauma with special reference to MTBI. The pathophysiological basis of persisting complaints, which are reported by a substantial subgroup of adult patients with MTBI, is far from clear. A computerised tomography (CT) examination is most often used to detect brain tissue damage in the acute setting. Nevertheless, it is generally considered that CT scanning and other neuroimaging techniques might be insensitive to minor structural and functional abnormalities and that there is a need for other, more sensitive methods. It has been suggested that biochemical markers such as the protein S 1 00B are useful, both for the acute diagnosis and to predict persistent complaints. In a prospective cohort of patients with a primarily uncomplicated MTBI, corresponding to an ordinary brain concussion, the mixed form S 1 00B as well as two more specific forms, S 1 00A 1 B and S 1001313, were analysed in sera in order to examine their diagnostic and predictive value. Serum concentrations of the specific form, S 1 00A 1 B, were elevated in 64% of the patients who had sustained an MTBI and the corresponding figure for the mixed form, S 1 00B, was 4 1 %, when compared to non-inj ured persons. Using a control group with mild orthopaedic injuries, S 1 00B did not differentiate the trauma groups, while S 1 00A1 B concentrations were significantly higher in the MTBI group (p<0.001). However, the diagnostic accuracy of S100A1B was not strong (sensitivity 64%, specificity 77% when the 97.5 percentile in healthy controls was used for cut-off). In contrast, S 1 00B more accurately identified the subgroup of patients with MTBI who had traumatic abnormalities on a CT scan or magnetic resonance images than S 1 00A 1 B did. We suggest that elevated serum concentrations of S 1 00A 1 B and S 1 00B respectively, reflect different pathophysiological mechanisms. Neither S 1 00A 1 B, nor S 1 00B predicted symptoms or signs of cognitive impairment. Serum concentrations of the specific form S 1 00BB were too low to draw any conclusion. The early, clinical follow-up of patients with MTBI must consider the risk of delayed intracranial complications. Data on the rate and risk factors of these complications are scarce. By conducting a case-control study, utilising the high-quality Inpatient Registry available in Sweden, we demonstrated that the rate of these complications in patients who have been discharged after uncomplicated, hospitalised observation, is low (0.13%) and that it declines during the first three weeks post-injury. Identified risk factors were clinical severity grade (OR 2.0 (Cl 1.2-3.6)) and male gender (OR 2.2 (Cl 1.4-3.5)). We could not demonstrate any protective effect of an early CT scan. TBI has long been considered a possible risk factor for brain tumour but previous studies have yielded inconsistent results. By conducting a population-based cohort study, utilising the Swedish Inpatient Registry as well as the Cancer Registry, we found evidence that TBI is not a risk factor for brain tumour (SIR 1.0 (Cl 0.9-1.2)).