Aim The aim of this study is to quantify visual field defects after temporal lobectomy for mesial temporal sclerosis and to establish eligibility for driving. Methods Automated static perimetry was performed on 14 patients who had undergone anterior temporal lobectomy for mesial temporal sclerosis. Perimetry consisted of monocular Humphrey Field Analyser (HFA) 30-2 test and a binocular Esterman 120 test. Results Of the 14 patients, three had no loss or non-specific loss, eight had partial homonymous quadrantanopia, one had complete homonymous quadrantanopia and two had concentric loss attributable to vigabatrin, which may have masked any loss occurring due to surgery. Of these, only seven passed the standardised DVLA visual fields. Of the seven who failed DVLA visual field, one had complete quadrantanopia, four had partial quadrantanopia and two had concentric loss (due to vigabatrin). Conclusions Visual field defects contribute a great deal in the reduction of the quality of life in patients who have had surgery for mesial temporal sclerosis. Potential surgically induced visual field defects that could preclude driving need to be discussed with each patient preoperatively. In our study 50% of patients did not meet the required DVLA standards.

The objective of the study was to highlight the diagnostic challenge of this elusive rare disease. A retrospective study of non-tuberculous spinal epidural abscesses (SEA) was carried out in Southern General Hospital, Glasgow, University Hospital of Wales, Cardiff, and Morriston Hospital, Swansea, from 1990 to 2000. Thirty-nine patients, consisting of 20 females and 19 males, with an age range from 20 to 85 years (mean: 61.1) were identified. Thirty-eight had localized back/neck pain. Eighteen were apyrexial. Twenty-nine demonstrated neurological deficit. All patients had raised inflammatory markers and gadolinium-enhanced magnetic resonance imaging (MRI) was diagnostic in 34. The most commonly identified organism was Staphylococcus aureus. All underwent surgical decompression, of which 13 required stabilization. Three died, seven lacked sphincter control and nine had motor deficit at the end of 1 year. It was concluded that fever is not mandatory for the diagnosis of SEA. Patients with localized back/neck pain and raised inflammatory markers need urgent MRI.

Antinbrinolytic treatment for 4 weeks after a subarachnoid hemorrhage has been shown to have no effect on outcome since a reduction in the rate of rebleeding was offset by an increase in ischemic events. To determine if a shorter course (4 days) of antinbrinolytic treatment before the expected onset of ischemic complications might reduce the rate of rebleeding yet avoid ischemic complications, we prospectively studied a series of 119 patients with subarachnoid hemorrhage; 479 patients with subarachnoid hemorrhage from our previous randomized double-blind study (238 treated with placebo, 241 with long-term tranexamic acid) served as historical control groups. At 3 months' follow-up, the outcome of patients treated with short-term tranexamic acid was not different from that of patients treated with long-term tranexamic acid. The rate of rebleeding (24 of 119, 20%) was near that with placebo (56 of 238, 24%). In contrast, the rate of cerebral infarction (33 of 119, 28%) was almost identical to that after long-term tranexamic acid (59 of 241, 24%), although mortality from cerebral infarction was reduced. Compared with historical control groups, treatment with tranexamic acid for 4 days fails to reduce the incidence of rebleeding but still increases the rate of cerebral infarction. {Stroke 1989;20:1674-1679)

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