Objective: To evaluate patient characteristics, symptoms, and examination findings in the clinical diagnosis of lumbosacral nerve root compression causing sciatica. Methods: The study involved 274 patients with pain radiating into the leg. All had a standardised clinical assessment and magnetic resonance (MR) imaging. The associations between patient characteristics, clinical findings, and lumbosacral nerve root compression on MR imaging were analysed. Results: Nerve root compression was associated with three patient characteristics, three symptoms, and four physical examination findings (paresis, absence of tendon reflexes, a positive straight leg raising test, and increased finger-floor distance). Multivariate analysis, analysing the independent diagnostic value of the tests, showed that nerve root compression was predicted by two patient characteristics, four symptoms, and two signs (increased finger-floor distance and paresis). The straight leg raise test was not predictive. The area under the curve of the receiver-operating characteristic was 0.80 for the history items. It increased to 0.83 when the physical examination items were added. Conclusions: Various clinical findings were found to be associated with nerve root compression on MR imaging. While this set of findings agrees well with those commonly used in daily practice, the tests tended to have lower sensitivity and specificity than previously reported. Stepwise multivariate analysis showed that most of the diagnostic information revealed by physical examination findings had already been revealed by the history items.

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Among patients with symptoms and signs of a lumbosacral radicular syndrome, bed rest is not a more effective therapy than watchful waiting.

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A series of 42 children is described who, following a seemingly minor or trivial head injury, developed neurological signs after a lucid or symptom-free period. This group constitutes 4.34 per cent of 967 consecutive patients aged 2 months to 17 years who were seen by members of the neurological staff during the years 1978-1981. Only one patient had an intracranial haematoma. The majority of patients showed a benign transient syndrome consisting of either convulsive or nonconvulsive signs with a spontaneous and full recovery. There were, however, 3 deaths in this series, apparently due to severe and uncontrollable unilateral or diffuse brain swelling, demonstrating the malignant counterpart of this benign syndrome. The theories seeking to explain these phenomena are reviewed. Special reference is made to the hypotheses of Bruce and his associates regarding brain swelling as a causative factor. It is considered that an adequate theory to explain the pathogenesis is still lacking. It is concluded that the juvenile brain responds to cranial trauma in a manner different from the adult brain. This implies a different approach in policy to hospital admission.