The first comprehensive in vivo documentation of the long term profile of pathological and spared tissue is described in a group of 10 patients with a diagnosis of herpes simplex encephalitis, who were left with memory difficulties as a major residual sequel of their condition. With a dedicated MRI protocol, which included high resolution images of temporal lobe and limbic system areas, data are provided on structures that have recently gained importance as anatomical substrates for amnesia. The major features of the lesion profile were: (1) unilateral or bilateral hippocampal damage never occurred in isolation, and was often accompanied by damage to the parahippocampus, the amygdala, specific temporal lobe gyri, and the temporal poles; (2) the insula was always abnormal; (3) neocortical temporal lobe damage was usually unilateral or asymmetric. It never occurred in isolation, and was invariably associated with more medial pathological changes; (4) anterior and inferior temporal lobe gyri were damaged more often and more severely than posterior and superior temporal lobe gyri; (5) pronounced abnormality was often present in the substantia innominata (region of the basal forebrain/anterior perforated substance); (6) there was evidence of significant abnormality in the fornix; (7) there was evidence of damage to the mammillary bodies; (8) thalamic nuclei were affected in around 50% of cases, with damage usually unilateral; (9) frontal lobe damage was present in a few patients, and affected medial areas more than dorsolateral areas; (10) there was some involvement of the striatum, although this was usually unilateral and mild; (11)

The effectiveness of spinal cord stimulation for control of spasticity was studied in 59 spinal cord injury patients. SCS was markedly or moderately effective in reducing spasticity in 63% of the patients. We found that control of spasticity by SCS was not correlated with the severity of spasticity, the type of spasticity (flexor or extensor), or the ability to ambulate. However, stimulation was more effective in patients with incomplete cervical lesions than in complete cervical lesions. Stimulation below the lesion was more effective than above. We conclude that SCS was effective when electrodes were properly positioned below the lesion over the posterior aspect of the spinal cord in patients with some residual spinal cord function. We hypothesize that SCS controls spasticity by modification of activity of spinal-brainstem-spinal loops and by suppression of segmental excitation through antidromic activation of propriospinal pathways.

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LS IllisStudy design: Review. Objectives: To examine the state of research in central nervous system (CNS) regeneration and to suggest an alternative to the sterile research at the lesion site. Setting: Worldwide. Methods: A search of publications using 'PubMed' and a search of the historical literature relevant to CNS regeneration, biological models, the neurone theory, collateral sprouting, spinal shock and the central pattern generator. Results: There is no evidence for CNS regeneration. Conclusion: A century of research focussed on the lesion site has been unproductive. An alternative field of research must be developed and the best candidate is the undamaged CNS.

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